Publications

@article{pmid38665057,

title = {Dampened circadian amplitude of EEG power in women after menopause},

author = {Rafael Pérez-Medina-Carballo and Anastasi Kosmadopoulos and Christophe Moderie and Philippe Boudreau and Manon Robert and Diane B Boivin},

doi = {10.1111/jsr.14219},

issn = {1365-2869},

year  = {2025},

date = {2025-08-01},

journal = {J Sleep Res},

volume = {34},

number = {4},

pages = {e14219},

abstract = {Postmenopausal women are at high risk of developing sleep-wake disturbances. We previously reported dampened circadian rhythms of melatonin, alertness and sleep in postmenopausal compared with young women. The present study aims to further explore electroencephalography power spectral changes in the sleep of postmenopausal women. Eight healthy postmenopausal women were compared with 12 healthy, naturally ovulating, young women in their mid-follicular phase. Participants followed a regular 8-hr sleep schedule for ≥ 2 weeks prior to laboratory entry. The laboratory visit included an 8-hr baseline sleep period followed by an ultradian sleep-wake cycle procedure, consisting of alternating 1-hr wake periods and nap opportunities. Electroencephalography power spectral analysis was performed on non-rapid eye movement sleep obtained over a 48-hr period. The baseline nocturnal sleep of postmenopausal women comprised lower power within delta and sigma, and higher power within alpha bands compared with that of younger women. During nighttime naps of the ultradian sleep-wake cycle procedure, lower power within delta and sigma, and higher power within beta bands were observed in postmenopausal women. During the ultradian sleep-wake cycle procedure, postmenopausal women presented lower power of delta, theta and sigma (14-15 Hz), undetectable rhythms of delta and theta, and a dampened or undetectable rhythm of sigma (12-15 Hz) power compared with younger women. Our results support the hypothesis of a dampened circadian variation of sleep microstructure in healthy-sleeping postmenopausal women. Circadian changes with aging are potential mechanisms for increased susceptibility to develop sleep disturbances; however, further research is needed to clarify their clinical implications and contribution to insomnia.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40354717,

title = {Internalizing symptoms and sleep disturbances associated with sleep bruxism in preschoolers},

author = {Christine Laganière and Nelly Huynh and Samantha Kenny and Hélène Gaudreau and Irina Pokhvisneva and Michael Meaney and Marie-Hélène Pennestri},

doi = {10.1016/j.sleep.2025.106553},

issn = {1878-5506},

year  = {2025},

date = {2025-08-01},

journal = {Sleep Med},

volume = {132},

pages = {106553},

abstract = {BACKGROUND AND OBJECTIVES: The presence of sleep bruxism (SB) has been associated with internalizing symptoms and sleep disturbances in school-aged children and adolescents. While manifestations of SB often start earlier in development, there is a lack of studies investigating such an association in younger age groups. Therefore, we assessed the association between SB frequency and (1) internalizing symptoms (anxiety and depression) and (2) sleep disturbances in preschoolers.nnMETHODS: The study comprised 340 mother-child dyads from a longitudinal cohort. Inclusion criteria were full-term pregnancy (>36 weeks), absence of birth complications, absence of severe health issues, and completion of essential measures for the present study. Mothers completed the Children's Sleep Habits Questionnaire when their child was four and five years old. Generalized estimating equation models were used to investigate our main objectives. The models included family socioeconomic status, child's sex, time, child's nighttime sleep duration, and maternal depressive symptoms as covariables.nnRESULTS: More frequent possible SB was associated with more anxiety (B = 0.682, p = 0.009) and depressive symptoms (B = 0.439, p = 0.02) in preschoolers. More frequent possible SB was also associated with more sleep anxiety (B = 0.450, p = 0.002) and bedtime resistance (B = 0.489, p = 0.01) but not with sleep onset delay, sleep duration, and night wakings (p > 0.05).nnCONCLUSIONS: Frequent possible SB episodes in preschoolers may be an indicator of depressive and anxiety difficulties during this developmental period. Bedtime manifestations of internalizing difficulties (bedtime resistance and sleep anxiety) paired with frequent SB in children should warrant further assessment for depressive and anxiety symptoms in preschoolers.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40460460,

title = {Symptom network connectivity indices as predictors of relapse in major depressive disorder},

author = {Abraham Nunes and Barbara Pavlova and John-Jose Nuñez and Lena C Quilty and Jane A Foster and Kate L Harkness and Keith Ho and Raymond W Lam and Qingqin S Li and Roumen Milev and Susan Rotzinger and Claudio N Soares and Valerie H Taylor and Gustavo Turecki and Sidney H Kennedy and Benicio N Frey and Frank Rudzicz and Rudolf Uher},

doi = {10.1016/j.psychres.2025.116562},

issn = {1872-7123},

year  = {2025},

date = {2025-08-01},

journal = {Psychiatry Res},

volume = {350},

pages = {116562},

abstract = {Major Depressive Disorder (MDD) demonstrates heterogeneous symptom profiles and a high relapse risk. Understanding how symptom interactions relate to relapse in MDD may enhance maintenance strategies. We thus investigated how connectivity in depressive symptom networks relates to relapse in MDD. We analyzed longitudinal data from 87 patients with remitted MDD who were followed for an average of 12 months. Patient-level symptom networks were estimated using multilevel graphical vector autoregression applied to weekly self-ratings of the Quick Inventory of Depressive Symptomatology. We calculated patient-specific network connectivity indices, including symptom network density (SND), vertex cover (VC) size, and minimal dominating set (MDS) size. Cox proportional hazards models assessed associations between these indices and time to relapse, controlling for baseline symptom severity. Higher SND and larger VC size were significantly associated with an increased relapse risk (HR for SND = 2.03, 95 % CI [1.44, 2.87], p < 0.001; HR for VC = 2.77, 95 % CI [1.79, 4.30], p < 0.001). Conversely, a larger MDS size was associated with a lower risk of relapse (HR 0.47, 95 % CI [0.31, 0.70], p < 0.001). Exploratory analyses showed that the strength centrality of sadness, difficulty concentrating, pessimism, suicidality, and low interest portend a higher relapse risk. Hyperconnectivity among depressive symptom networks may indicate vulnerability to relapse in MDD. Our results further support the potential utility of symptom network-based analyses for predicting outcomes in MDD. Future studies should evaluate whether symptom network-based analyses can provide markers for personalized treatment planning.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40347524,

title = {Longitudinal relationships among cerebrospinal fluid biomarkers, cerebral blood flow, and grey matter volume in individuals with a familial history of Alzheimer's disease},

author = {Safa Sanami and Brittany Intzandt and Julia Huck and Sylvia Villeneuve and Yasser Iturria-Medina and Claudine J Gauthier and Prevent-Ad Research Group},

doi = {10.1016/j.neurobiolaging.2025.04.011},

issn = {1558-1497},

year  = {2025},

date = {2025-08-01},

journal = {Neurobiol Aging},

volume = {152},

pages = {43--53},

abstract = {Alzheimer's disease (AD) is a complex disease that involves complex interactions between protein biomarkers such as amyloid beta (Aβ) and tau, neurodegeneration, cerebrovascular health and inflammation. However, how these factors interact, especially in the early phases of disease development remain unclear. To address this, this study analyzed four-year longitudinal data from 110 cognitively unimpaired older adults with a family history of AD in the PreventAD cohort. We investigated relationships between CSF Aβ, 181-phosphorylated tau (p-tau), interleukin-8 (IL-8), cerebral blood flow (CBF), and grey matter volume (GMV) in groups with high and low cardiovascular risk levels. Longitudinally, lower CSF Aβ within participants (a proxy for higher brain amyloid) was linked to a slower decline in regional CBF, particularly in those with higher cardiovascular risk. Similarly, in the high vascular risk group, higher IL-8 at baseline was associated with greater decline in CBF in the right superior temporal gyrus. Further, lower baseline CBF was associated with greater CSF p-tau accumulation over time. Finally, higher baseline CSF p-tau was associated with faster GM atrophy over 4 years, particularly in the hippocampus. Our results highlight the complex interactions between CSF misfolded proteins, inflammatory markers, and brain regional CBF and atrophy, and how these effects are more pronounced in individuals with higher vascular risk factor load. These findings demonstrate the need for comprehensive models of AD pathophysiology that integrate vascular health and inflammation measures alongside traditional biomarkers.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40382867,

title = {Social and mental health pathways to institutional trust: A cohort study},

author = {Vincent Paquin and Diana Miconi and Samantha Aversa and Janique Johnson-Lafleur and Sylvana Côté and Marie-Claude Geoffroy and Sinan Gülöksüz},

doi = {10.1016/j.socscimed.2025.118199},

issn = {1873-5347},

year  = {2025},

date = {2025-08-01},

journal = {Soc Sci Med},

volume = {379},

pages = {118199},

abstract = {OBJECTIVE: Trust in institutions such as the government is lower in the context of mental health problems and socio-economic disadvantage. However, the roles of structural inequality, interpersonal factors, and mental health on institutional trust remain unclear. This study aimed to examine the associations of social and mental health factors, from early life to adulthood, with institutional trust.nnMETHOD: Participants (n = 1347; 57.2 % female) were from the population-based Québec Longitudinal Study of Child Development (1997-2021). Trust in 13 institutions was self-reported at age 23. Predictors were 20 social and mental health factors during early life, adolescence, and adulthood. Associations were examined with linear regressions corrected for false discovery rate. Pathways were explored using the temporal Peter-Clark algorithm.nnRESULTS: Early-life factors associated with lower levels of trust were male sex, racialized minority status, low household income, and maternal history of depression and antisocial behaviors. After adjusting for early-life factors, adolescence factors associated with lower levels of trust were internalizing and externalizing problems, bullying exposure, and school difficulties. Independently of early-life or adolescence factors, adulthood factors associated with lower levels of trust were perceived stress, psychotic experiences, suicidal ideas, and seeking professional help, whereas greater social connectedness was associated with greater trust. Temporal Peter-Clark analyses identified social connectedness and psychotic experiences as potential proximal determinants of institutional trust.nnCONCLUSION: This study identified factors related to structural inequality, interpersonal relationships, and mental health over development that were associated with institutional trust. Interventions aimed at promoting social connectedness and equity may improve institutional trust and wellbeing.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40413924,

title = {From resting-state functional hippocampal centrality to functional outcome: An extended neurocognitive model of psychosis},

author = {Jana F Totzek and Jai L Shah and Alexandra L Young and Ashok Malla and Ridha Joober and Delphine Raucher-Chéné and Martin Lepage and Katie M Lavigne},

doi = {10.1016/j.psychres.2025.116538},

issn = {1872-7123},

year  = {2025},

date = {2025-08-01},

journal = {Psychiatry Res},

volume = {350},

pages = {116538},

abstract = {BACKGROUND: We previously proposed a neurocognitive model of psychosis in which reduced morphometric hippocampal-cortical connectivity precedes impaired episodic memory, social cognition, negative symptoms, and functional outcome. We provided support for this model in a patient subtype, and aimed to extend these findings to resting-state functional MRI to potentially explain the progression for a broader range of patients.nnMETHODS: We used a subsample of our previous analysis consisting of 54 patients with first-episode psychosis and 52 controls and applied the machine-learning algorithm Subtype and Stage Inference, which combines clustering and disease progression modeling, to the patient data for rs-functional hippocampal connectivity, episodic memory, social cognition, negative symptoms and functioning.nnRESULTS: We identified three subtypes, with Subtype 0 being unimpaired on the markers, Subtype 1 showing impaired hippocampal connectivity and episodic memory, and Subtype 2 showing impaired memory and a trend for impaired functioning. We identified similar progression patterns to our previously published morphometric results in functional MRI data (hippocampal dysconnectivity preceded cognition, symptoms, and functioning in one subtype and followed these alterations in another subtype). We further show that the impairments in our previously published and current findings across modalities do not necessarily overlap in patients, hinting towards an additive effect of morphometric and resting-state connectivity in explaining the neurocognitive underpinnings of this model.nnCONCLUSION: Our results provide an extension of our previous work and build the foundation for a multimodal neurocognitive model of psychosis, potentially elucidating this aspect of illness progression in psychosis for a broader range of patients.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40158843,

title = {Fatty acid amide hydrolase in comorbid borderline personality disorder and major depressive disorder: Imaging with [C]CURB PET},

author = {Michelle A De Pol and Dorsa Rafiei and Jeffrey H Meyer and Kimberly L Desmond and Shelley McMain and Isabelle Boileau and Jerry Warsh and Pablo Rusjan and Christian Schmahl and Neil Vasdev and Lauren R Gray and Ryan Aloysius and Nathan J Kolla},

doi = {10.1016/j.neuropharm.2025.110436},

issn = {1873-7064},

year  = {2025},

date = {2025-08-01},

journal = {Neuropharmacology},

volume = {273},

pages = {110436},

abstract = {Borderline personality disorder (BPD) is highly comorbid with major depressive disorder (MDD), and the comorbid condition is associated with poorer treatment outcomes, which necessitates the investigation of transdiagnostic biomarkers. Previous research suggests that fatty acid amide hydrolase (FAAH), an endocannabinoid enzyme, is elevated in the prefrontal cortex (PFC) in BPD; however, no study has examined FAAH density in individuals with comorbid conditions. We hypothesized that FAAH level would be elevated in the prefrontal cortex, anterior cingulate cortex and hippocampus of comorbid BPD + MDD compared to healthy controls, as these brain regions are linked to the pathobiology of both disorders. For an exploratory analysis, we hypothesized that brain FAAH would be positively correlated with symptom severity, aggression, and impulsivity. Fifteen unmedicated BPD + MDD cases and 15 age- and sex-matched healthy controls underwent a [C]CURB positron emission tomography scan to measure λk, an index of available FAAH. No significant group differences in [C]CURB λk were observed between BPD + MDD patients and controls. Negative correlations were found between [C]CURB λk and physical aggression scores in the dorsolateral PFC (r = -0.64, p = 0.04), ventrolateral PFC (r = -0.75, p = 0.01), medial PFC (r = -0.64, p = 0.03), and orbitofrontal cortex (r = -0.66, p = 0.03) in the BPD + MDD group. A positive correlation was found between [C]CURB λk and impulsivity, as measured by the Barratt Impulsiveness Scale-11, in the ventrolateral PFC (r = 0.62, p = 0.04) of the BPD + MDD group. We suggest that the negative correlations between [C]CURB λk and physical aggression could reflect a relationship between FAAH and planned aggression whereas the latter findings may reflect a positive relationship with impulsivity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40619893,

title = {Early Psychosis Symptoms Noted by Family Physicians in Electronic Medical Records During Help-Seeking Visits in Primary Care: Symptômes précoces de psychose relevés par les médecins généralistes dans les dossiers médicaux électroniques lors de consultations en soins primaires pour demande d'aide},

author = {Joshua C Wiener and Rebecca Rodrigues and Jennifer N S Reid and Suzanne Archie and Saadia Hameed Jan and Arlene G MacDougall and Lena Palaniyappan and Liisa Jaakkimainen and Branson Chen and Neo Sawh and Kelly K Anderson and },

doi = {10.1177/07067437251355637},

issn = {1497-0015},

year  = {2025},

date = {2025-07-01},

journal = {Can J Psychiatry},

pages = {7067437251355637},

abstract = {BackgroundThe objectives of this study were (1) to describe the symptoms noted by family physicians during help-seeking visits for early psychosis, relative to a validated screening tool for early psychosis in primary care, and (2) to examine the referral disposition of patients meeting the screening tool cut-off.MethodsWe constructed a retrospective cohort of Ontario residents aged 14-35 years with an incident diagnosis of non-affective psychotic disorder between 2005-2015 in health administrative data, and at least one visit in the Electronic Medical Record Primary Care database during the 6 months prior to the date of psychotic disorder diagnosis ( = 572). We abstracted symptoms of psychosis noted by the family physician in the electronic medical records and compared these to the Primary Care Checklist (PCCL) for early psychosis.ResultsThe most frequent PCCL items noted were "tension or nervousness" (13.3%), "depressive mood" (12.5%), "increased stress or deterioration in functioning" (7.5%), and "sleep difficulties" (6.6%). The PCCL cut-off was met by 187 patients (33%) across 327 visits (8%). A greater proportion of visits meeting the PCCL cut-off had psychosis noted as the main presenting issue (55.4% vs. 6.8%) and resulted in referral to mental health services (33.3% vs. 6.0%) than those not meeting the cut-off. However, two in three visits where the screening cut-off for early psychosis was met did not result in a referral to mental health services.DiscussionThe findings of this study suggest that family physicians may benefit from a screening tool when early psychosis is suspected to improve identification and guide referral practices.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39694537,

title = {Neonatal estradiol and early adversity interact to modify basolateral amygdala morphology and adult behavior in female rats},

author = {Grace Kraatz and Henry Tian Hao Xie and Hong Long and Claire-Dominique Walker},

doi = {10.1111/jne.13483},

issn = {1365-2826},

year  = {2025},

date = {2025-07-01},

journal = {J Neuroendocrinol},

volume = {37},

number = {7},

pages = {e13483},

abstract = {Being raised under adverse conditions during infancy and childhood represents a significant risk factor for developing later psychopathologies and dysfunctions in emotional, affective, and cognitive abilities. Depending on the type, timing, and duration of early adversity, different consequences emerge across the sexes in both human and animal models, although our understanding of the underlying interactions between sex and early life stress (ELS) is still incomplete. In this study, we used the limited bedding (LB) paradigm, a well-described model of ELS in rat pups during the first 10 days of life, and tested whether masculinization of the female brain by neonatal injections of estradiol benzoate (EB) would recapitulate the ELS-induced vulnerability phenotype of males on morphology of the basolateral amygdala (BLA) principal neurons and pre-adolescent and adult behavior. Our results show that LB-induced morphological changes in BLA neurons of weaning female rats were eliminated by EB treatment independently of early changes in estrogen receptor (ERα) expression in this region. EB treatment synergized with LB to enhance play behavior of pre-adolescent females to levels far greater than those observed in control males. In adult offspring, LB reduced time spent in the center in males and EB tended to increase social contact time compared to normal females, but only in LB conditions. Our findings indicate that neonatal masculinization of the female brain modifies specific, but not all aspects of BLA morphology and both pre-adolescent and adult behavior that are altered by ELS.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39984680,

title = {Resting-state fMRI reveals altered functional connectivity associated with resilience and susceptibility to chronic social defeat stress in mouse brain},

author = {Derek Lupinsky and Md Taufiq Nasseef and Carine Parent and Kelly Craig and Josie Diorio and Tie-Yuan Zhang and Michael J Meaney},

doi = {10.1038/s41380-025-02897-2},

issn = {1476-5578},

year  = {2025},

date = {2025-07-01},

journal = {Mol Psychiatry},

volume = {30},

number = {7},

pages = {2943--2954},

abstract = {Chronic stress is a causal antecedent condition for major depressive disorder and associates with altered patterns of neural connectivity. There are nevertheless important individual differences in susceptibility to chronic stress. How functional connectivity (FC) amongst interconnected, depression-related brain regions associates with resilience and susceptibility to chronic stress is largely unknown. We used resting-state functional magnetic resonance imaging (rs-fMRI) to examine FC between established depression-related regions in susceptible (SUS) and resilient (RES) adult mice following chronic social defeat stress (CSDS). Seed-seed FC analysis revealed that the ventral dentate gyrus (vDG) exhibited the greatest number of FC group differences with other stress-related limbic brain regions. SUS mice showed greater FC between the vDG and subcortical regions compared to both control (CON) or RES groups. Whole brain vDG seed-voxel analysis supported seed-seed findings in SUS mice but also indicated significantly decreased FC between the vDG and anterior cingulate area compared to CON mice. Interestingly, RES mice exhibited enhanced FC between the vDG and anterior cingulate area compared to SUS mice. Moreover, RES mice showed greater FC between the infralimbic prefrontal cortex and the nucleus accumbens shell compared to CON mice. These findings indicate unique differences in FC patterns in phenotypically distinct SUS and RES mice that could represent a neurobiological basis for depression, anxiety, and negative-coping behaviors that are associated with exposure to chronic stress.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40619281,

title = {Preliminary Investigation of the Association Between Epigenetic Aging Acceleration and Amyloid Biomarkers in Bipolar Disorder},

author = {Gabriel R Fries and Steven De La Garza and Ning O Zhao and Andres W Bass and Camila N C Lima and Nobuhide Kobori and Tatiana Barichello and Gustavo Turecki and Paul E Schulz and Breno S Diniz and Jair C Soares},

doi = {10.1016/j.jagp.2025.06.008},

issn = {1545-7214},

year  = {2025},

date = {2025-07-01},

journal = {Am J Geriatr Psychiatry},

abstract = {OBJECTIVES: Bipolar disorder (BD) has been associated with an elevated risk of Alzheimer's Disease (AD). We assessed AD biomarkers in BD and tested whether epigenetic aging (EA) acceleration is associated with changes in these markers.nnDESIGN, SETTING, PARTICIPANTS: Cross-sectional study of n = 58 living individuals with BD and n = 20 age- and sex-matched control participants, as well as analyses of postmortem brain samples (Brodmann area 9/46) from n = 46 individuals with BD.nnMEASUREMENTS: Amyloid beta (Aβ), Aβ, and total Tau levels were measured in plasma from individuals with BD and controls, and Aβ levels were measured in brains. EA and its acceleration (blood: GrimAge and DunedinPACE; brains: DNAmClock) were estimated for all samples. Individuals with BD were split into quartiles with slower or accelerated EA if they were in the first or fourth quartiles for GrimAge acceleration (AgeAccelGrim), DunedinPACE, or DNAmClock acceleration (DNAmClockAccel).nnRESULTS: Individuals with BD showed a decrease in the Aβ ratio (p = 0.048) compared to controls, and a significant decrease in the Aβ ratio was also found in individuals with BD with high versus low AgeAccelGrim (p = 0.048). Brain Aβ levels significantly correlated with DNAmClockAccel (r = 0.270, p = 0.007), with those with high EA acceleration showing higher brain Aβ after controlling for confounders (p = 0.008).nnCONCLUSIONS: Our results provide preliminary evidence that accelerated EA is associated with markers of AD in individuals with BD, suggesting it as a potential target in efforts to prevent dementia and AD in BD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39923816,

title = {Transcriptional and Neurochemical Signatures of Cerebral Blood Flow Alterations in Individuals With Schizophrenia or at Clinical High Risk for Psychosis},

author = {Samuel R Knight and Leyla Abbasova and Yashar Zeighami and Justine Y Hansen and Daniel Martins and Fernando Zelaya and Ottavia Dipasquale and Thomas Liu and David Shin and Matthijs Bossong and Matilda Azis and Mathilde Antoniades and Oliver D Howes and Ilaria Bonoldi and Alice Egerton and Paul Allen and Owen O'Daly and Philip McGuire and Gemma Modinos},

doi = {10.1016/j.biopsych.2025.01.028},

issn = {1873-2402},

year  = {2025},

date = {2025-07-01},

journal = {Biol Psychiatry},

volume = {98},

number = {2},

pages = {144--155},

abstract = {BACKGROUND: The brain integrates multiple scales of description, from the level of cells and molecules to large-scale networks and behavior. Understanding relationships across these scales may be fundamental to advancing understanding of brain function in health and disease. Recent neuroimaging research has shown that functional brain alterations that are associated with schizophrenia spectrum disorders (SSDs) are already present in young adults at clinical high risk for psychosis (CHR-P), but the cellular and molecular determinants of these alterations remain unclear.nnMETHODS: Here, we used regional cerebral blood flow (rCBF) data from 425 individuals (122 with an SSD compared with 116 healthy control participants [HCs] and 129 individuals at CHR-P compared with 58 HCs) and applied a novel pipeline to integrate brainwide rCBF case-control maps with publicly available transcriptomic data (17,205 gene maps) and neurotransmitter atlases (19 maps) from 1074 healthy volunteers.nnRESULTS: We identified significant correlations between astrocyte, oligodendrocyte, oligodendrocyte precursor cell, and vascular leptomeningeal cell gene modules for both SSD and CHR-P rCBF phenotypes. Additionally, endothelial cell genes were correlated in SSD, and microglia in CHR-P. Receptor distribution significantly predicted case-control rCBF differences, with dominance analysis highlighting dopamine (D, D, dopamine transporter), acetylcholine (VAChT, M), gamma-aminobutyric acid A (GABA), and glutamate (NMDA) receptors as key predictors for SSD (R = 0.58, false discovery rate [FDR]-corrected p < .05) and CHR-P (R = 0.6, p < .05) rCBF phenotypes. These associations were primarily localized in subcortical regions and implicate cell types involved in stress response and inflammation, alongside specific neuroreceptor systems, in shared and distinct rCBF phenotypes in psychosis.nnCONCLUSIONS: Our findings underscore the value of integrating multiscale data as a promising hypothesis-generating approach toward decoding biological pathways involved in neuroimaging-based psychosis phenotypes, potentially guiding novel interventions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40615152,

title = {Universal, selective and indicated parenting interventions to prevent the development of adverse mental health outcomes in youth: a meta-review of systematic reviews},

author = {Meredith X Han and Edward Chesney and Valerie Ng and Joanna Bright and Yashna K Sagar and Ellie Baker and Michael J Meaney and Evelyn C Law},

doi = {10.1136/bmjment-2025-301613},

issn = {2755-9734},

year  = {2025},

date = {2025-07-01},

journal = {BMJ Ment Health},

volume = {28},

number = {1},

abstract = {BACKGROUND: Preventive interventions in the form of parenting support can reduce the risk of mental disorders in children. Summarising the effectiveness of parenting interventions across different levels of prevention can inform the prioritisation of the intervention.nnOBJECTIVES: We conducted a meta-review of systematic reviews and meta-analyses on universal, selective and indicated parenting interventions to prevent adverse mental health outcomes in youth.nnSTUDY SELECTION AND ANALYSIS: PubMed, Ovid, Embase and PsycNet were searched. Systematic reviews consisting of randomised controlled trials of preventative parenting interventions were included. We provided a narrative synthesis of the results and assessed the quantity and quality of evidence for each level of prevention (ie, universal, selective, indicated) and mental health outcome.nnFINDINGS: We identified 32 systematic reviews and meta-analyses, which included 354 randomised controlled trials, consisting of over 74 558 children and adolescents. Universal parenting interventions were effective in delaying the initiation of alcohol and cannabis use, but did not have consistent findings in preventing disruptive behaviour and mood disorders. Selective interventions were predominantly beneficial for disruptive behavioural problems across a variety of risk factors. Indicated interventions found substantial and consistent evidence for reducing problems in children with behavioural problems. Caution is warranted when interpreting findings, as the overall confidence rating of most reviews was very low, especially in the reporting of study selection and justifying exclusions in the AMSTAR-2.nnCONCLUSIONS: Our findings highlight the need for robust evidence synthesis. Despite the limitations of the current evidence base, parenting interventions hold promise for preventing mental health disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40118225,

title = {Large-scale effects of prenatal inflammation and early life circadian disruption in mice: Implications for neurodevelopmental disorders},

author = {Tara C Delorme and Danusa M Arcego and Danae Penichet and Nicholas O'Toole and Nikki Huebener and Patrícia P Silveira and Lalit K Srivastava and Nicolas Cermakian},

doi = {10.1016/j.bbi.2025.03.023},

issn = {1090-2139},

year  = {2025},

date = {2025-07-01},

journal = {Brain Behav Immun},

volume = {127},

pages = {409--422},

abstract = {Around 80 % of individuals with neurodevelopmental disorders such as schizophrenia and autism spectrum disorders experience disruptions in sleep/circadian rhythms. We explored whether environmental circadian disruption interacts with prenatal infection, a risk factor for neurodevelopmental disorders, to induce sex-specific deficits in mice. A maternal immune activation (MIA) protocol was used by injecting pregnant mice with viral mimic poly IC or saline at E9.5. Juvenile/adolescent male and female offspring (3-7 weeks old) were then subjected to a standard light:dark cycle (12:12LD) or to constant light (LL). Significant interactions between treatment (MIA, control) and lighting (12:12LD, LL) were evident in behaviors related to cognition, anxiety, and sociability. This pattern persisted in our RNA sequencing analysis of the dorsal hippocampus, where poly IC exposure resulted in numerous differentially expressed genes (DEGs) in males, while exposure to both poly IC and LL led to a marked reduction in DEGs. Through WGCNA analysis, many significant gene modules were found to be positively associated with poly IC (vs. saline) and LL (vs. LD) in males (fewer in females). Many of the identified hub-bottleneck genes were homologous to human genes associated with sleep/circadian rhythms and neurodevelopmental disorders as revealed by GWA studies. The MIA- and LL-associated modules were enriched in microglia gene signatures, which was paralleled by trends of effects of each of the factors on microglia morphology. In conclusion, in a mouse model of prenatal infection, circadian disruption induced by LL during adolescence acts as a modulator of the effects of MIA at behavioral, cellular, and molecular levels.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40583230,

title = {Physical Mechanisms of Emotions Evoked by Postural Feedback},

author = {Soren Wainio-Theberge and Ignacio Spiousas and Jorge L Armony},

doi = {10.1111/psyp.70095},

issn = {1469-8986},

year  = {2025},

date = {2025-07-01},

journal = {Psychophysiology},

volume = {62},

number = {7},

pages = {e70095},

abstract = {Adopting physical expressions of emotion has been shown to have feedback effects on individuals' mood and behavior. For example, adopting the expansive and contractive body language of dominance and submission can affect individuals' feelings of power. However, the effects can be subtle and variable; we suggest that this may be due to inter-individual variability in the physical expression of the experimental posture, including both the magnitude of the posture adopted and the specific muscles used to adopt it. Here, we employed a postural feedback (i.e., "power posing") paradigm and recorded quantitative measures of body position algorithmically derived from video recordings (N = 101). We demonstrate for the first time that variation in neck flexion mediates the effects of posture on mood. We also investigated several other variables which, based on previous work, could additionally mediate or moderate the postural feedback effects, finding that subjective difficulty also mediates posture effects independently of neck flexion, with effects moderated by body awareness. Finally, we investigated the muscular processes underlying neck flexion in the posture using electromyography, demonstrating that the neck flexion which mediates mood effects is associated with sternocleidomastoid muscle activity. The present work carries implications for our understanding of the adaptive benefits of expansive and contractive postures, and provides important methodological insights into the paradigms typically used for research on postural feedback.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40620111,

title = {The Neural Correlates of Delusions in Dementia: A Scoping Review},

author = {Adèle Gagnon and Bryn H Manns and Karina Atanasiu and Dominique Lumley and Mallar Chakravarty and Serge Gauthier and Ian Gold},

doi = {10.1111/psyg.70060},

issn = {1479-8301},

year  = {2025},

date = {2025-07-01},

journal = {Psychogeriatrics},

volume = {25},

number = {4},

pages = {e70060},

abstract = {Delusions are common symptoms of dementia and are clinically significant. The objective of this scoping review is to identify possible neural correlates. MEDLINE (OVID), EMBASE (OVID) and Web of Science were searched in December 2020 for the keywords 'delusions' and 'dementia'. Two informal searches were carried out subsequently. Results were limited to those in English. Intervention and study characteristics were extracted using standardised tools. Eighteen published studies, using four distinct experimental methods, were included, and 31 brain regions were identified as correlates of delusions. No region was identified consistently within included studies or found in more than four studies. Despite the range of brain regions identified, a number form part of the default mode network, the salience network or the central executive network. We explore the implications of these findings for understanding delusions in dementia.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40605462,

title = {Accuracy of blood-based neurofilament light to different genetic frontotemporal dementia from primary psychiatric disorders},

author = {Ella Liu and Sherri Lee Jones and Victoria Light and Charlotte Teunissen and Arabella Bouzigues and Lucy L Russell and Phoebe H Foster and Eve Ferry-Bolder and John C van Swieten and Lize C Jiskoot and Harro Seelaar and Raquel Sanchez-Valle and Robert Laforce and Caroline Graff and Daniela Galimberti and Rik Vandenberghe and Alexandre de Mendonça and Pietro Tiraboschi and Isabel Santana and Alexander Gerhard and Johannes Levin and Sandro Sorbi and Markus Otto and Chris R Butler and Isabelle Le Ber and Elizabeth Finger and Maria Carmela Tartaglia and Mario Masellis and James B Rowe and Matthis Synofzik and Fermin Moreno and Barbara Borroni and Henrik Zetterberg and Jonathan D Rohrer and Simon Ducharme and },

doi = {10.1177/13872877251352103},

issn = {1875-8908},

year  = {2025},

date = {2025-07-01},

journal = {J Alzheimers Dis},

pages = {13872877251352103},

abstract = {BackgroundGenetic frontotemporal dementia (FTD) along with Alzheimer's disease (AD), is one of the most prevalent early-onset dementias. The differential diagnosis of FTD from primary psychiatric disorder (PPD) has been challenging due to significant symptom overlap, particular as FTD often presents with prolonged psychiatric prodromes.ObjectiveThis study aims to evaluate whether blood-based neurofilament light chain (NfL) can differentiate genetic FTD from PPD, and to determine a global clinical cutoff to differentiate genetic FTD carriers from PPD with high specificity and sensitivity.MethodsData (ages 40-81) were obtained from FTD mutation carriers (GENFI;  = 474;  = 120   114  = 50 ,  = 190 controls), and PPD (Biobanque Signature;  = 848). Blood-based NfL was measured with SIMOA HD-X (BbS) and SIMOA HD-1 (GENFI).ResultsBlood-based NfL was higher in all symptomatic mutations compared to PPD. Mildly symptomatic (0 < FTLD CDR-SOB-NM < 4)  and  carriers also had higher NfL. ROC curve revealed an optimal blood-based NfL cutoff of 22.1 pg/mL ( = 0.647) to distinguish symptomatic genetic FTD from PPD (78.5% sensitivity, 86.2% specificity, AUC = 0.908). For mildly symptomatic subjects, a cutoff of 16.2 pg/mL ( = 0.601) differentiated groups with 86.7% sensitivity and 73.5% specificity (AUC = 0.870).ConclusionsNfL holds potential as a blood-based biomarker for symptomatic genetic FTD carriers, with moderate accuracy to distinguish PPD from mild forms including .},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39526850,

title = {Putative risk and resiliency factors after an augmented training program for preventing posttraumatic stress injuries among public safety personnel from diverse sectors},

author = {Juliana M B Khoury and Taylor A Teckchandani and Jolan Nisbet and Sherry H Stewart and Gordon J G Asmundson and Tracie O Afifi and Michelle C E McCarron and Gregory P Kratzig and Shannon Sauer-Zavala and J Patrick Neary and Renée S MacPhee and Alain Brunet and Terence M Keane and R Nicholas Carleton},

doi = {10.1080/16506073.2024.2420636},

issn = {1651-2316},

year  = {2025},

date = {2025-07-01},

journal = {Cogn Behav Ther},

volume = {54},

number = {4},

pages = {457--476},

abstract = {Mental health disorders are particularly prevalent among public safety personnel (PSP). Emotional Resilience Skills Training (ERST) is a cognitive behavioural training program for PSP based on the Unified Protocol for the Transdiagnostic Treatment of Emotional Disorders (i.e. Unified Protocol). The current study was designed to assess whether ERST is associated with reduced putative risk factors for mental disorders and increased individual resilience. The PSP-PTSI Study used a longitudinal prospective sequential experimental cohort design that engaged each participant for approximately 16 months. PSP from diverse sectors (i.e. firefighters, municipal police, paramedics, public safety communicators) completed self-report measures of several putative risk variables (i.e. anxiety sensitivity, fear of negative evaluation, pain anxiety, illness and injury sensitivity, intolerance of uncertainty, state anger) and resilience at three time points: pre-training ( = 191), post-training ( = 103), and 1-year follow-up ( = 41). Participant scores were statistically compared across time points. Participants reported statistically significantly lower scores on all putative risk variables except pain anxiety, and statistically significantly higher resilience from pre- to post-training. Changes were sustained at 1-year follow-up. The results indicate that ERST is associated with reductions in several putative risk variables and improvement in resilience among PSP.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39827219,

title = {Novel synaptic markers predict early tau pathology and cognitive deficit in an asymptomatic population at risk of Alzheimer's disease},

author = {Jiarui Ao and Cynthia Picard and Daniel Auld and Henrik Zetterberg and Ann Brinkmalm and Kaj Blennow and Sylvia Villeneuve and John C S Breitner and Judes Poirier and },

doi = {10.1038/s41380-024-02884-z},

issn = {1476-5578},

year  = {2025},

date = {2025-07-01},

journal = {Mol Psychiatry},

volume = {30},

number = {7},

pages = {2810--2820},

abstract = {Cognitive dysfunction in Alzheimer's disease (AD) correlates closely with pathology in the neuronal microtubule-associated protein tau. Tau pathology may spread via neural synapses. In a population of cognitively unimpaired elderly at elevated risk of AD, we investigated four cerebrospinal (CSF) markers of synaptic dysfunction and degeneration. Three of these (SYT1, SNAP25, and ADAM23) are derived from pre-synaptic structures, while ADAM22 reflects post-synaptic changes. All four markers correlated strongly with tau protein measures. In statistical models, SYT1 accounted for more than half the total variance in both total- and P(181)-tau levels. Observed correlations with CSF levels of Alzheimer amyloid-β (Aβ42) were somewhat weaker. In longitudinal data, baseline levels of ADAM22 and ADAM23 robustly predicted increase over time in both total- and P-tau. CSF SYT1 levels also correlated with PET image uptake of tau and (at a trend level) Aβ in areas of interest for early AD pathology. CSF SYT1 and SNAP25 levels correlated inversely with a global psychometric score and several of its domain subscales. In quantitative trait loci analyses, all four synaptic markers were associated with at least one AD genetic risk locus. Upon "staging" participants by their evidence of amyloid and tau pathology (A/T/N framework), the CSF synaptic markers were unexpectedly reduced in participants with CSF evidence of amyloid but not tau pathology. They were clearly elevated, however, in the CSF of persons with indications of both tau and amyloid pathology. These observations provide evidence for clear pre-synaptic degeneration in cognitively unimpaired persons with biomarker evidence of early AD pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40156272,

title = {Polygenic Risk Score Analysis of Antidepressant Treatment Outcomes: A CAN-BIND-1 Study Report: Analyse des résultats du traitement antidépresseur à l'aide des scores de risque polygéniques : Rapport sur l'étude CAN-BIND-1},

author = {Leen Magarbeh and Samar S M Elsheikh and Farhana Islam and Victoria S Marshe and Xiaoyu Men and Emytis Tavakoli and Martin Kronenbuerger and Stefan Kloiber and Benicio N Frey and Roumen Milev and Claudio N Soares and Sagar V Parikh and Franca Placenza and Stefanie Hassel and Valerie H Taylor and Francesco Leri and Pierre Blier and Rudolf Uher and Faranak Farzan and Raymond W Lam and Gustavo Turecki and Jane A Foster and Susan Rotzinger and Sidney H Kennedy and Daniel J Müller},

doi = {10.1177/07067437251329073},

issn = {1497-0015},

year  = {2025},

date = {2025-07-01},

journal = {Can J Psychiatry},

volume = {70},

number = {7},

pages = {552--564},

abstract = {ObjectiveThe genetic architecture of antidepressant response is poorly understood. This study investigated whether polygenic risk scores (PRSs) for major psychiatric disorders and a personality trait (neuroticism) are associated with antidepressant treatment outcomes.MethodsWe analysed 148 participants with major depressive disorder (MDD) from the Canadian Biomarker Integration Network for Depression-1 (CAN-BIND-1) cohort. Participants initially received escitalopram (ESC) monotherapy for 8 weeks. Nonresponders at week 8 received augmentation with aripiprazole (ARI), while responders continued ESC until week 16. Primary outcomes were remission status and symptom improvement measured at weeks 8 and 16. At week 16, post-hoc stratified analyses were performed by treatment arm (ESC-only vs. ESC + ARI). Eleven PRSs derived from genome-wide association studies of psychiatric disorders (e.g., MDD and post-traumatic stress syndrome (PTSD)) and neuroticism, were analysed for associations with these outcomes using logistic and linear regression models.ResultsAt week 8, a higher PRS for PTSD was nominally associated with a lower probability of remission (odds ratio (OR) = 0.08 [0.014-0.42], empirical -value = 0.017) and reduced symptom improvement (beta (standard error) = -29.15 (9.76), empirical -value = 0.019). Similarly, a higher PRS for MDD was nominally associated with decreased remission probability (OR = 0.38 [0.18-0.78], empirical -value = 0.044). However, none of the results survived multiple testing corrections. At week 16, the stratified analysis for the ESC-only group revealed that a higher PRS for MDD was associated with increased remission probability (empirical value = 0.034) and greater symptom improvement (empirical -value = 0.02). In contrast, higher PRSs for schizophrenia (empirical -value = 0.013) and attention-deficit hyperactivity disorder (empirical -value = 0.032) were associated with lower symptom improvement. No significant associations were observed in the ESC + ARI group.ConclusionsThese findings suggest that PRSs may influence treatment outcomes, particularly in ESC monotherapy. Replication in larger studies is needed to validate these observations.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40601344,

title = {Mental Health Antecedents and Correlates of 2 Distinct Developmental Pathways to Suicidal Ideation},

author = {Marie-Claude Geoffroy and Sasha MacNeil and Vincent Paquin and Ayla Inja and Alain Girard and Élise Chartrand and Natalie Castellanos-Ryan and Charles-Édouard Notredame and Ian Colman and Massimiliano Orri and Gustavo Turecki and Sylvana Côté},

doi = {10.1001/jamapsychiatry.2025.1273},

issn = {2168-6238},

year  = {2025},

date = {2025-07-01},

journal = {JAMA Psychiatry},

abstract = {IMPORTANCE: Suicidal ideation is increasingly common in youth. Trajectories and associated mental health symptoms across development remain poorly understood.nnOBJECTIVE: To describe trajectories of suicidal ideation from early adolescence to young adulthood and identify preceding and co-occurring mental health symptoms to inform optimal prevention.nnDESIGN, SETTING, AND PARTICIPANTS: This cohort study used data from a contemporary, longitudinal cohort study, the Québec Longitudinal Study of Child Development (QLSCD), including reports from participants, parents, and teachers. The QLSCD is a population-based birth cohort study of 2120 singletons born between 1997 and 1998 in Québec, Canada, and followed up to age 25 years (2023). Data were analyzed from September 2024 to February 2025.nnMAIN OUTCOMES AND MEASURES: Serious suicidal ideation in the past 12 months was assessed by a question to participants at ages 13, 15, 17, 20, 23, and 25 years.nnEXPOSURES: Mental health symptoms (eg, internalizing, externalizing) as reported by parents, teachers, and self-reports on validated questionnaires and standardized across 5 developmental periods: preschool (3-5 years), childhood (6-12 years), early adolescence (13 years), mid-late adolescence (15-17 years), and young adulthood (20-25 years).nnRESULTS: A total of 1635 participants (845 female [51.7%]; participant number is weighted to account for selective attrition) provided answers on suicidal ideation, with survey weights applied. A total of 3 trajectories were identified: minimal/no ideation (1433 [87.6%]), onset in early adolescence (117 [7.1%]), and onset in young adulthood (86 [5.2%]). Relative to minimal/no ideation, onset in early adolescence was associated with elevated symptoms across nearly all mental health indicators from childhood through adulthood. This included both internalizing (eg, childhood depressive symptoms: risk ratio [RR], 1.75; 95% CI, 1.45-2.05) and externalizing (eg, childhood disruptive symptoms: RR, 1.60; 95% CI, 1.29-1.91) symptoms and maternal antisocial symptoms (RR, 1.39; 95% CI, 1.11-1.66). In contrast, onset of suicidal ideation in young adulthood was associated with internalizing symptoms (eg, mid-late adolescence depressive symptoms: RR, 1.84; 95% CI, 1.28-2.39) emerging in adolescence and worsening mental distress in young adulthood.nnCONCLUSIONS AND RELEVANCE: Results of this cohort study revealed 2 pathways to suicidal ideation: onset in early adolescence, with persistent childhood internalizing/externalizing symptoms, and onset in young adulthood linked to internalizing symptoms emerging in adolescence without prior distress. Findings suggest timely addressing of mental health symptoms and developmental stage-specific prevention.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40590827,

title = {Suicide Ideation During Adolescence and Predictors for Its Trajectories: A 6-Year Follow-Up Study in Korea},

author = {Tianna Loose and Léa Perret and Minjae Choi and Marie-Claude Geoffroy and Duckyoung Chon and Jihee Kim and Myung Ki},

doi = {10.1016/j.jadohealth.2025.05.014},

issn = {1879-1972},

year  = {2025},

date = {2025-07-01},

journal = {J Adolesc Health},

abstract = {PURPOSE: Suicide ideation experienced by adolescents may persist over time but is also subject to change. With due consideration of the changing nature of suicide ideation in adolescents, we aimed to identify the trajectories of suicide ideation and the protective and risk factors associated with each trajectory.nnMETHODS: This study used a 6-year follow-up cohort of adolescents (n = 2,205) who were aged 13 years, first-year middle school students at baseline, from the Korean Children and Youth Panel Study. We conducted growth mixture modeling to characterize trajectories of suicide ideation, which were measured at four time points over the middle and high school periods. Using multinomial logistic regression, we analyzed a wide range of factors in relation to suicide ideation trajectories with adjustment for demographic and behavioral characteristics.nnRESULTS: Suicide ideation reached a peak in the third year of middle school (15.7% at age 15). Three different trajectories (low, transient, and persistent) were identified. Depressive symptoms, maltreatment, and low self-esteem were associated with greater risk of both transient and persistent suicide ideation trajectories, but with a higher magnitude of association for the persistent trajectory. When transient and persistent trajectories were compared, depressive symptoms (odds ratio [OR] = 1.45, 95% confidence interval [CI] = 1.08-1.94), cell phone dependency (OR = 1.20, 95% CI = 0.96-1.50), and self-esteem (OR = 0.79, 95% CI = 0.61-1.02) were differentiated two trajectories.nnDISCUSSION: Similar protective and risk factors were associated with both transient and persistent suicide ideation but with stronger associations for persistent trajectories. Self-esteem, maltreatment, and depression may act as a broad-spectrum intervention point to target both transient and persistent suicide ideation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40593718,

title = {Glial reactivity correlates with synaptic dysfunction across aging and Alzheimer's disease},

author = {Francieli Rohden and Pamela C L Ferreira and Bruna Bellaver and João Pedro Ferrari-Souza and Cristiano S Aguzzoli and Carolina Soares and Sarah Abbas and Hussein Zalzale and Guilherme Povala and Firoza Z Lussier and Douglas T Leffa and Guilherme Bauer-Negrini and Nesrine Rahmouni and Cécile Tissot and Joseph Therriault and Stijn Servaes and Jenna Stevenson and Andrea L Benedet and Nicholas J Ashton and Thomas K Karikari and Dana L Tudorascu and Henrik Zetterberg and Kaj Blennow and Eduardo R Zimmer and Diogo Souza and Pedro Rosa-Neto and Tharick A Pascoal},

doi = {10.1038/s41467-025-60806-1},

issn = {2041-1723},

year  = {2025},

date = {2025-07-01},

journal = {Nat Commun},

volume = {16},

number = {1},

pages = {5653},

abstract = {Previous studies suggest glial and neuronal changes may trigger synaptic dysfunction in Alzheimer's disease (AD), but the link between their markers and synaptic abnormalities in the living brain remains unclear. We investigated the association between glial reactivity and synaptic dysfunction biomarkers in cerebrospinal fluid (CSF) from 478 individuals in cognitively unimpaired (CU) and cognitively impaired (CI) individuals. We measured amyloid-β (Aβ), phosphorylated tau (pTau181), astrocyte reactivity (GFAP), microglial activation (sTREM2), and synaptic markers (GAP43, neurogranin). CSF GFAP levels were associated with presynaptic and postsynaptic dysfunction, independent of cognitive status or Aβ presence. CSF sTREM2 levels were related to presynaptic markers in cognitively unimpaired and impaired Aβ+ individuals, and to postsynaptic markers in cognitively impaired Aβ+ individuals. Notably, CSF pTau mediated the relationships between GFAP or sTREM2 and synaptic dysfunction. Our findings, validated in two independent cohorts (TRIAD and ADNI), reveal a distinct pattern of glial contribution to synaptic degeneration.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40440822,

title = {The inventory of psychotic-like anomalous self-experiences (IPASE): Stability and relationships with attenuated psychotic symptoms and remission in individuals at-risk for psychosis},

author = {Isabelle Scott and Alexandra Selloni and Zarina Bilgrami and Matthew Cotter and Cansu Sarac and Alessia McGowan and Marija Krcmar and Melanie Formica and Kate Gwyther and Cassandra Wannan and Agrima Srivastava and Guillermo A Cecchi and Romina Mizrahi and Patrick McGorry and Cheryl M Corcoran and Barnaby Nelson},

doi = {10.1016/j.schres.2025.05.003},

issn = {1573-2509},

year  = {2025},

date = {2025-07-01},

journal = {Schizophr Res},

volume = {281},

pages = {286--294},

abstract = {BACKGROUND: The IPASE is a self-report measure of basic self-disturbance, a core feature of schizophrenia and ultra-high risk (UHR) states. However, the extent to which basic self-disturbance-as captured by the IPASE-is stable over time and related to the severity or progression of attenuated psychotic symptoms (APS) remains unclear. We examined the temporal stability of IPASE scores, their correlation with APS, and whether they predict changes in APS over time.nnMETHODS: The baseline sample included 185 participants (healthy controls = 72, UHR = 66, first-episode psychosis = 47), with 29 UHR participants re-assessed at month-12. Correlations between IPASE scores and Comprehensive Assessment of At-Risk Mental States (CAARMS) positive symptom scores were evaluated at baseline and month-12. Stability between baseline and month-12 IPASE scores was examined in the longitudinal subsample. Regression was used to predict remission and change in CAARMS scores.nnRESULTS: Although mean IPASE scores were significantly higher in the UHR group compared to HCs, total IPASE scores were only weakly correlated with CAARMS total scores (ρ=0.27). IPASE subscales showed weak correlations (0.08<ρ<0.27) with CAARMS positive symptom domains. Changes in IPASE and CAARMS scores were not correlated. Moderate stability was found for IPASE total scores (ICC = 0.59) and four subscales (0.58 < ICC < 0.64), excluding the cognition subscale (ICC = 0.3). Baseline IPASE scores did not predict remission (partial R=0.05) or change in CAARMS scores (partial R=0.02).nnCONCLUSION: The IPASE is a moderately stable measure in UHR individuals, correlates with the presence of positive psychotic symptoms but only weakly with severity, and does not strongly predict positive symptom change.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40598470,

title = {Brain state dynamics and working memory in patients with schizophrenia and unaffected siblings},

author = {Feiwen Wang and Jie Yang and Jun Yang and Peng Cheng and Wenjian Tan and Danqing Huang and Maoxing Zhong and Xiawei Liu and Weiqing Huang and Zhening Liu and Lena Palaniyappan},

doi = {10.1186/s12916-025-04216-6},

issn = {1741-7015},

year  = {2025},

date = {2025-07-01},

journal = {BMC Med},

volume = {23},

number = {1},

pages = {376},

abstract = {BACKGROUND: Working memory (WM) deficits are a key feature of schizophrenia and are also seen in unaffected siblings. These deficits might arise  from disrupted transitions from one brain state to another. Using a robust algorithm called the Bayesian Switching Dynamical System (BSDS), we studied hidden brain states and their transitions during a WM task in people with schizophrenia.nnMETHODS: We used BSDS to identify brain states based on regions of interest (ROIs) within the default mode network and the frontoparietal network in 161 patients with schizophrenia, 37 unaffected siblings, and 96 healthy controls during N-back (0, 2, and resting fixation) tasks. We estimated group differences in the properties of brain states and studied the influence of WM performance and clinical characteristics on them using General Linear Models.nnRESULTS: We identified 4 brain states underlying the WM task: high-demand, low-demand, fixation, and non-dominant states. Compared with controls and siblings, patients showed reduced occupancy and lifetime of high-demand state during the "2-back," reduced lifetime of low-demand state during the "0-back," but increased occupancy and lifetime of fixation state during both task periods. Aberrant high-demand state mediated the association between WM performance and negative symptoms. Compared with controls and patients, siblings showed increased occupancy of high-demand and reduced fixation state during the resting fixation condition; this putative compensatory process correlated with better WM performance.nnCONCLUSIONS: Latent brain states of intrinsic connectivity that represent internal mental processes affect WM performance, influencing the expression of negative symptoms in schizophrenia and cognitive resilience in unaffected siblings.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40290196,

title = {Exposure to Fine Particulate Matter During Pregnancy Is Associated With Hippocampal Development in Offspring},

author = {Jessica L Buthmann and Tarik Benmarhnia and Jonathan Y Huang and Pei Huang and Jonas G Miller and Jessica P Uy and Peter D Gluckman and Marielle V Fortier and Yap-Seng Chong and Ai Peng Tan and Michael J Meaney and Ian H Gotlib},

doi = {10.1016/j.bpsgos.2025.100490},

issn = {2667-1743},

year  = {2025},

date = {2025-07-01},

journal = {Biol Psychiatry Glob Open Sci},

volume = {5},

number = {4},

pages = {100490},

abstract = {BACKGROUND: As the global climate crisis persists, it becomes increasingly important to understand how exposure to environmental toxins can affect the developing brain. Although researchers are beginning to document links between prenatal exposure to air pollution and brain structure, it is not clear when these associations emerge.nnMETHODS: We leveraged data from the GUSTO (Growing Up Toward Healthy Outcomes in Singapore) longitudinal birth cohort study to examine prenatal exposure to air pollution and brain development during childhood. Spatiotemporally interpolated prenatal exposure to particulate matter <2.5 μm was averaged across each prenatal week. Structural magnetic resonance imaging data were obtained when children were ages 4.5, 6.0, 7.5, and 10.5 years ( = 325, 47.7% female) and segmented with FreeSurfer 7.1. A subset of parents completed the Child Behavior Checklist at the final assessment ( = 195, 46.7% female). We used latent growth modeling to estimate a slope of hippocampal volume growth in each hemisphere from ages 4.5 to 10.5 years, adjusted for intracranial volume.nnRESULTS: Distributed lag models indicated that late gestational exposure (during weeks 36-40) was associated with slower hippocampal growth in both hemispheres. Importantly, we also found that faster hippocampal volume growth in the right hemisphere was associated with more externalizing and attention problems at 10.5 years.nnCONCLUSIONS: Future research should examine mechanisms that may underlie or contribute to these associations. These findings underscore the importance of efforts to reduce pollution, particularly for pregnant people and their children.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40519638,

title = {Peripheral MicroRNA Signatures in Adolescent Depression},

author = {Alice Morgunova and Nicholas O'Toole and Fatme Abboud and Saché Coury and Gary Gang Chen and Maxime Teixeira and Eamon Fitzgerald and Gustavo Turecki and Anthony J Gifuni and Ian H Gotlib and Corina Nagy and Michael J Meaney and Tiffany C Ho and Cecilia Flores},

doi = {10.1016/j.bpsgos.2025.100505},

issn = {2667-1743},

year  = {2025},

date = {2025-07-01},

journal = {Biol Psychiatry Glob Open Sci},

volume = {5},

number = {4},

pages = {100505},

abstract = {BACKGROUND: Adolescent depression is linked to enduring maladaptive outcomes, chronic severity of symptoms, and poor treatment response. Identifying epigenetic signatures of adolescent depression is urgently needed to improve early prevention and intervention strategies. MicroRNAs (miRNAs) are epigenetic regulators of adolescent neurodevelopmental processes, but their role as markers and mediators of adolescent depression is unknown.nnMETHODS: Here, we examined miRNA profiles from dried blood spot samples of male and female adolescents with clinical depression and psychiatrically healthy male and female adolescents ( = 62). We processed and sequenced these samples using a small RNA protocol tailored for miRNA identification.nnRESULTS: We identified 9 differentially expressed (DE) miRNAs (adjusted  value < .05), all of which were upregulated in adolescents with depression. At future follow-ups post blood collection, expression of miR-3613-5p, mir-30c-2, and miR-942-5p were positively associated with depression severity but not anxiety, suggesting a stronger link to persistent depression symptoms. Expression of miR-32-5p inversely correlated with hippocampal volume, highlighting a potential neurobiological basis. Common predicted gene targets of the DE miRNAs are involved in neurodevelopment, cognitive processing, and depressive disorders.nnCONCLUSIONS: These findings lay the groundwork for identifying adolescent peripheral miRNA markers that reflect neurodevelopmental pathways that shape lifelong psychopathology risk.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40518731,

title = {Aggression, Suicidality, and Emotion Profiles in Youth: Links to Early Life Adversity},

author = {Erinn Acland and Nina Pocuca and Sophie Chaput-Langlois and Jad Hamaoui and Julie Girard-Lapointe and Sylvana Côté and Natalie Castellanos-Ryan and Marie-Claude Geoffroy},

doi = {10.1002/ab.70038},

issn = {1098-2337},

year  = {2025},

date = {2025-07-01},

journal = {Aggress Behav},

volume = {51},

number = {4},

pages = {e70038},

abstract = {Suicidality and physical aggression are leading, related youth public health concerns. Yet, whether adolescents who harm themselves, others, or both differ emotionally and etiologically remains unclear. To address this, adolescents from a prospective population-based birth cohort reported their suicidality, physical aggression, depression/anxiety symptoms, anger, and callousness (N = 1637). Distinct latent harm-emotion profiles were identified, which were linked to perinatal and childhood experiences. A six-profile solution was retained: Low harm (79.5%), moderate suicidality (6.5%), high suicidality (2%), high aggression (2.5%), moderate aggression (8.5%), and high suicidality and aggression (dual harm; 1%). Elevated harm profiles were compared to the low-harm group. Moderate/high suicidality profiles showed slight elevations in physical aggression. All elevated harm profiles expressed higher negative emotionality. Dual harm and aggression groups reported higher callousness, while suicidality groups reported lower callousness. Aggression profiles were 75% male, suicidality profiles were 21% male, while the low and dual-harm profiles were more similarly mixed sex (47% vs. 63% male, respectively). Low-harm youth experienced more positive childhood parenting. The dual harm and high aggression groups had more deviant childhood best friends, while the dual harm and moderate aggression groups had lower early life household income. The moderate suicidality group had fathers with higher depressive symptoms during infancy and childhood. Thus, one in five youth showed relatively elevated suicidality and/or physical aggression; of which, 95% tended to have a primary target (themselves or others). Early life economic, parental, and peer support may be key for preventing suicidal and aggressive outcomes in adolescence.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40522652,

title = {Frequency and Clinical Outcomes Associated With Tau Positron Emission Tomography Positivity},

author = {Alexis Moscoso and Fiona Heeman and Sheelakumari Raghavan and Alejandro Costoya-Sánchez and Martijn van Essen and Ismini Mainta and Valle Camacho and Omar Rodríguez-Fonseca and Jesús Silva-Rodríguez and Andrés Perissinotti and Yuna Gu and Jihwan Yun and Debora Peretti and Federica Ribaldi and Emma M Coomans and Wagner S Brum and Michel J Grothe and Pablo Aguiar and Gérard N Bischof and Alexander Drzezga and Sang Won Seo and Sylvia Villeneuve and Maura Malpetti and John T O'Brien and James B Rowe and Elsmarieke M van de Giessen and Rik Ossenkoppele and William J Jagust and Ruben Smith and Oskar Hansson and Giovanni B Frisoni and Valentina Garibotto and David N Soleimani-Meigooni and Maria Carrillo and Bradford C Dickerson and Renaud La Joie and Gil D Rabinovici and Liana G Apostolova and Pamela J LaMontagne and Michael J Pontecorvo and Keith A Johnson and Reisa A Sperling and Michael W Weiner and Ronald C Petersen and Clifford R Jack and Prashanthi Vemuri and Michael Schöll and },

doi = {10.1001/jama.2025.7817},

issn = {1538-3598},

year  = {2025},

date = {2025-06-01},

journal = {JAMA},

abstract = {IMPORTANCE: Tau positron emission tomography (PET) allows in vivo detection of neurofibrillary tangles, a core neuropathologic feature of Alzheimer disease (AD).nnOBJECTIVE: To provide estimates of the frequency of tau PET positivity and its associated risk of clinical outcomes.nnDESIGN, SETTING, AND PARTICIPANTS: Longitudinal study using data pooled from 21 cohorts, comprising a convenience sample of 6514 participants from 13 countries, collected between January 2013 and June 2024. Cognitively unimpaired individuals and patients with a clinical diagnosis of mild cognitive impairment (MCI), AD dementia, or other neurodegenerative disorders were included.nnEXPOSURES: Tau PET with flortaucipir F 18, amyloid-β (Aβ) PET, and clinical examinations. Tau PET scans were visually rated as positive according to a US Food and Drug Administration- and European Medicines Agency-approved method, designed to indicate the presence of advanced neurofibrillary tangle pathology (Braak stages V-VI).nnMAIN OUTCOMES AND MEASURES: Frequency of tau PET positivity and absolute risk of clinical progression (eg, progression to MCI or dementia).nnRESULTS: Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years. Of 3487 cognitively unimpaired participants, 349 (9.8%) were tau PET positive; the estimated frequency of tau PET positivity was less than 1% in those aged younger than 50 years, and increased from 3% (95% CI, 2%-4%) at 60 years to 19% (95% CI, 16%-24%) at 90 years. Tau PET positivity frequency estimates increased across MCI and AD dementia clinical diagnoses (43% [95% CI, 41%-46%] and 79% [95% CI, 77%-82%] at 75 years, respectively). Most tau PET-positive individuals (92%) were also Aβ PET positive. Cognitively unimpaired participants who were positive for both Aβ PET and tau PET had a higher absolute risk of progression to MCI or dementia over the following 5 years (57% [95% CI, 45%-71%]) compared with both Aβ PET-positive/tau PET-negative (17% [95% CI, 13%-22%]) and Aβ PET-negative/tau PET-negative (6% [95% CI, 5%-8%]) individuals. Among participants with MCI at the time of the tau PET scan, an Aβ PET-positive/tau PET-positive profile was associated with a 5-year absolute risk of progression to dementia of 70% (95% CI, 59%-81%).nnCONCLUSIONS AND RELEVANCE: In a large convenience sample, a positive tau PET scan occurred at a nonnegligible rate among cognitively unimpaired individuals, and the combination of Aβ PET positivity and tau PET positivity was associated with a high risk of clinical progression in both preclinical and symptomatic stages of AD. These findings underscore the potential of tau PET as a biomarker for staging AD pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40495109,

title = {General Practitioners' Management of Individuals with Gambling Disorder: A Systematic Review of Practices, Knowledge, Attitudes and Beliefs},

author = {Ovidiu Tatar and Veronica Iammatteo and Magaly Brodeur and Marie-Josée Fleury},

doi = {10.1007/s10899-025-10402-1},

issn = {1573-3602},

year  = {2025},

date = {2025-06-01},

journal = {J Gambl Stud},

abstract = {Gambling disorder (GD) has a significant impact on individuals, the healthcare system, and the society. The vast majority of individuals with GD do not use healthcare services for their GD. Since primary care is the first point of contact, exploring barriers to GD treatment is of utmost importance. For this systematic review, we searched five major databases up to October 2024 and included empirical studies describing the practices of general practitioners (GPs) and emergency department physicians regarding GD, as well as their knowledge, attitudes, and beliefs about GD management. We retained six quantitative and six qualitative articles that reported GP data on GD management; however, no studies conducted in emergency departments met our inclusion criteria. The narrative synthesis revealed that none of the GPs routinely screened for GD, only 7-14% treated GD themselves, and approximately half referred these individuals to mental health specialists. While more than half of GPs were knowledgeable about GD-related harms, only 17-38% were confident in their knowledge of GD or care pathways. Although over 65% acknowledged their potential role in managing GD, multiple barriers to care were identified. These included negative attitudes, such as attributing gambling-related harms to individual character weakness, insufficient training on GD screening tools and treatment modalities, and the low prioritization of GD treatment within the healthcare system. Given the higher risk of GD among individuals with mental health disorders (e.g., depression, anxiety) and substance use disorders, prioritizing GD screening and treatment for these high-risk groups in primary care is essential.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40502575,

title = {Gray matter microstructure from in-vivo diffusion MRI reflects post-mortem neuropathology severity and clinical progression of Alzheimer's disease},

author = {Zaki Alasmar and Cécilia Tremblay and Roqaie Moqadam and Geidy E Serrano and Thomas G Beach and Alizera Atri and Yi Su and Yashar Zeighami and Mahsa Dadar},

doi = {10.1101/2025.05.30.25328630},

year  = {2025},

date = {2025-06-01},

journal = {medRxiv},

abstract = {INTRODUCTION: Diffusion-weighted imaging derived mean diffusivity (MD) correlates with Alzheimer's disease biomarkers, yet its neuropathological correlates remain unclear.nnMETHODS: Diffusion-weighted imaging, postmortem neuropathology, and cognitive performance data were obtained from the National Alzheimer's Coordinating Center (N=97), Alzheimer's Disease Neuroimaging Initiative (N=21), and Arizona Study of Aging and Neurodegenerative Disorders (N=15). We examined MD associations with neuropathology, cognitive decline, and expression profiles of AD-implicated genes.nnRESULTS: Results revealed two latent variables-one linked to amyloid/tau, the other to vascular pathology-explaining 70% and 16% of MD-pathology covariance, respectively. Higher MD correlated with worse cognitive performance, both cross-sectionally and up to 14 years prior to death. MD was regionally associated with Thal phase, neuritic plaque density, Braak stage (temporal/limbic), and infarcts (thalamus), and reflected gene expression patterns related to AD.nnDISCUSSION: In vivo MD captures distinct AD-related pathologies across brain regions and relates to cognitive trajectories and gene expression.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40202728,

title = {Convergence of Cannabis and Psychosis on the Dopamine System},

author = {Jessica Ahrens and Sabrina D Ford and Betsy Schaefer and David Reese and Ali R Khan and Philip Tibbo and Rachel Rabin and Clifford M Cassidy and Lena Palaniyappan},

doi = {10.1001/jamapsychiatry.2025.0432},

issn = {2168-6238},

year  = {2025},

date = {2025-06-01},

journal = {JAMA Psychiatry},

volume = {82},

number = {6},

pages = {609--617},

abstract = {IMPORTANCE: Despite evidence that individuals with a cannabis use disorder (CUD) are at elevated risk of psychosis and that the neurotransmitter dopamine has a role in psychosis, the mechanism linking cannabis use and psychosis remains unclear.nnOBJECTIVE: To use neuromelanin-sensitive magnetic resonance imaging (MRI), referred to as the neuromelanin-MRI signal, a practical, proxy measure of dopamine function, to assess whether a common alteration in the dopamine system may be implicated in CUD and psychosis and whether this alteration can be observed in those with a CUD whether or not they have a diagnosis of first-episode schizophrenia (FES).nnDESIGN, SETTING, AND PARTICIPANTS: This longitudinal observational cohort study recruited individuals from 2019 to 2023 from an early psychosis service and the surrounding communities in London, Ontario. The sample included individuals with and without CUD, with some in each group also diagnosed with FES.nnEXPOSURES: FES and CUD diagnoses from the Structured Clinical Interview for DSM-5.nnMAIN OUTCOMES AND MEASURES: Neuromelanin-MRI signals within the midbrain (substantia nigra [SN]/ventral tegmental area [VTA]) including a subregion previously linked to the severity of untreated psychosis (a priori region of interest). Linear mixed-effects analyses were performed relating neuromelanin-MRI signals to clinical measures.nnRESULTS: A total of 36 individuals without CUD (mean [SD] age, 22.3 [3.2] years; 29 male [81%]; 12 with FES) and 25 individuals with CUD (mean [SD] age, 24.3 [4.7] years; 22 male [88%]; 16 with FES) participated in the study. One-year follow-up was completed for 12 individuals with CUD and 25 without CUD. CUD was associated with elevated neuromelanin-MRI signal in a set of ventral SN/VTA voxels (387 of 2060 SN/VTA voxels, corrected P = .03, permutation test). CUD was also associated with elevated neuromelanin-MRI signal in the psychosis-related region of interest (t92 = 2.12, P = .04) with a significant dose-dependent association (higher burden of CUD symptoms associated with higher neuromelanin-MRI signal, F1, 96 = 4.89; P = .03). In contrast, participants with FES did not exhibit a significant elevation in neuromelanin-MRI signal (241 SN/VTA voxels had elevated signal, corrected P = .09). There was no association between time and neuromelanin-MRI signal.nnCONCLUSIONS AND RELEVANCE: Elevated dopamine function in a critical SN/VTA subregion may be associated with psychosis risk in people with CUD. Cannabis was associated with the hypothesized final common pathway for the clinical expression of psychotic symptoms.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40502602,

title = {Vascular risk factors mediate the relationship between education and white matter hyperintensities},

author = {Shima Raeesi and Yashar Zeighami and Roqaie Moqadam and Cassandra Morrison and Mahsa Dadar},

doi = {10.1101/2025.06.03.25328899},

year  = {2025},

date = {2025-06-01},

journal = {medRxiv},

abstract = {INTRODUCTION: Education can protect against cognitive decline and dementia through cognitive reserve and reduced vascular risk. This study examined whether vascular risk mediates the relationship between education and white matter hyperintensity (WMH) burden.nnMETHODS: Data from 1089 older adults from the National Alzheimer's Coordinating Center were analyzed. A composite vascular score was created using diabetes, hypertension, hypercholesterolemia, smoking, alcohol abuse, body mass index, and blood pressure. Linear regressions and mediation analyses examined associations and indirect effects between education, vascular risk, and WMH, adjusting for age, sex, and diagnosis.nnRESULTS: Higher education was associated with lower vascular risk ( < .001) and WMH burden ( = .01). Mediation analysis showed an indirect effect of education on WMH via vascular risk (a*b = -0.02,  = .004), accounting for 23% of the total effect.nnDISCUSSION: Education influences cerebrovascular health via reducing vascular risk. Addressing vascular health may reduce WMH burden.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40199794,

title = {Exploring the power of MRI and clinical measures in predicting AD neuropathology},

author = {Farooq Kamal and Cassandra Morrison and Michael D Oliver and Mahsa Dadar},

doi = {10.1007/s11357-025-01645-2},

issn = {2509-2723},

year  = {2025},

date = {2025-06-01},

journal = {Geroscience},

volume = {47},

number = {3},

pages = {5003--5023},

abstract = {Predicting Alzheimer's disease (AD) pathology prior to clinical diagnosis is important for identifying individuals at high risk of developing AD dementia. However, there remains a gap in leveraging MRI and clinical data to predict AD pathology. This study examines a novel machine learning approach that integrates the combined vascular (white matter hyperintensities, WMHs) and structural brain changes (gray matter, GM) with clinical factors (cognitive scores) to predict post-mortem neuropathology. Participants from the Alzheimer's Disease Neuroimaging Initiative dataset (ADNI) and National Alzheimer's Coordinating Center (NACC) with both post-mortem neuropathology data and antemortem MRI and clinical data were included. Machine learning models were applied towards feature selection of the top seven MRI, clinical, and demographic data to identify the best performing set of variables that could predict postmortem neuropathology outcomes (i.e., neurofibrillary tangles, neuritic plaques, diffuse plaques, senile/amyloid plaques, and amyloid angiopathy). The best-performing neuropathology predictors from ADNI were then validated in NACC to compare results and ensure that the feature selection process did not lead to overfitting. In ADNI, the best-performing model included total and temporal lobe WMHs and achieved r = 0.87(RMSE = 0.62) during cross-validation for neuritic plaques. Overall, post-mortem neuropathology outcomes were predicted up to 14 years before death with high accuracies (~ 90%). Similar results were observed in the NACC dataset. These findings highlight that MRI features are critical to successfully predict AD-related pathology years in advance.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40505888,

title = {Neurite Density and Kurtosis in the Gray Matter of People with Early Schizophrenia},

author = {Peter C Van Dyken and Ali R Khan and Lena Palaniyappan},

doi = {10.1016/j.bpsc.2025.06.001},

issn = {2451-9030},

year  = {2025},

date = {2025-06-01},

journal = {Biol Psychiatry Cogn Neurosci Neuroimaging},

abstract = {BACKGROUND: Classical models of diffusion weighted imaging, especially diffusion tensor imaging, are unsuited for application to the cortical gray matter, given the regions high microstructural complexity. As such, most neuroimaging studies thus far have focused on gross structural effects of schizophrenia, such as cortical thickness differences. More recently developed models, such as the neurite orientation dispersion and density imaging (NODDI) model and diffusion kurtosis imaging (DKI), incorporate higher resolution data and may provide more sensitive descriptions of schizophrenia pathology with more specific interpretations.nnMETHODS: We applied the NODDI and DKI models to the cortical gray matter of people with early schizophrenia (n=54) and healthy controls (n=51) from the Human Connectome Project - Early Psychosis dataset. Comparisons between groups were made using region-of-interest and clustering approaches. The effect sizes of these approaches were compared to those of cortical thickness differences. We also investigated the relationship between these parameters and lifetime antipsychotic usage.nnRESULTS: Cortical thickness differences were most prominent between groups in terms of global effect size and spatial extent. We also observed a diffuse, right-hemisphere dominant increase in mean kurtosis and isotropic diffusion fraction throughout the gray matter, not fully explained by partial volume effects. Additionally, a lower neurite density index (NDI) correlated with greater lifetime antipsychotic usage.nnCONCLUSIONS: Increases in mean kurtosis and isotropic diffusion fraction are both markers of schizophrenia, consistent with inflammation models of the gray matter in schizophrenia. NDI reduction, reflecting intraneurite pathology, becomes prominent only in those with greater disease burden.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40506005,

title = {Selective insensitivity to global vs. local linguistic context in speech produced by patients with untreated psychosis and positive thought disorder},

author = {Victoria Sharpe and Michael Mackinley and Samer Nour Eddine and Lin Wang and Lena Palaniyappan and Gina R Kuperberg},

doi = {10.1016/j.biopsych.2025.06.001},

issn = {1873-2402},

year  = {2025},

date = {2025-06-01},

journal = {Biol Psychiatry},

abstract = {BACKGROUND: Early psychopathologists proposed that certain features of positive thought disorder, the disorganized language output produced by some people with schizophrenia, suggest an insensitivity to global, relative to local, discourse context. This idea has received support from carefully controlled psycholinguistic studies in language comprehension. In language production, researchers have so far remained reliant on subjective qualitative rating scales to assess and understand speech disorganization. Now, however, recent advances in large language models mean that it is possible to quantify sensitivity to global and local context objectively by probing lexical probability (the predictability of a word given its preceding context) during natural language production.nnMETHODS: For each word in speech produced by 60 first-episode psychosis patients and 35 healthy, demographically-matched controls, we extracted lexical probabilities from GPT-3 based on contexts that ranged from very local- a single preceding word: P(Wn | Wn-1)-to global-up to 50 preceding words: P(Wn|Wn-50, Wn-49, …, Wn-1).nnRESULTS: We show that disorganized speech is characterized by disproportionate insensitivity to global, versus local, linguistic context. Critically, this global-versus-local insensitivity selectively predicted clinical ratings of positive thought disorder, above and beyond overall symptom severity. There was no evidence of a relationship with negative thought disorder (impoverishment).nnCONCLUSIONS: We provide an automated, interpretable measure that can potentially be used to quantify speech disorganization in schizophrenia. Our findings directly link the clinical phenomenology of thought disorder to neurocognitive constructs that are grounded in psycholinguistic theory and neurobiology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40544541,

title = {Implementation of a digital measurement-based care approach in an early intervention service for psychosis: the PEPP-Montreal electronic data capture protocol and its alignment with learning health system principles},

author = {Elissa Zavaglia and Ridha Joober and Srividya N Iyer and Kevin MacDonald and Martin Lepage and Sherezad Abadi and Jai Shah and Manuela Ferrari},

doi = {10.1016/j.schres.2025.05.021},

issn = {1573-2509},

year  = {2025},

date = {2025-06-01},

journal = {Schizophr Res},

volume = {282},

pages = {141--149},

abstract = {Measurement-based care, crucial for improving outcomes in psychiatric disorders, remains underutilized, particularly during the impactful early treatment phases. Inspired by a learning health system approach, a hybrid paper/electronic data capture platform was developed at PEPP-Montreal, an early psychosis program, gathering data on patient socio-demographics, symptoms, functioning, pathways to care, substance use, and medication monitoring. This article evaluates the year-one deployment of this innovative infrastructure (2022-2023). The novel 2022 hybrid infrastructure was compared with the 2016 paper-based version, using the RE-AIM framework (Reach, Effectiveness, Adoption, Implementation, and Maintenance). Phase 1 identified evidence-based clinical measures including patient-reported, clinician-reported, and evaluator-reported outcomes, while phase 2 further streamlined and implemented the electronic data capture platform. Continuous data collection through the platform was deployed at six time points. Results included: Reach: N = 53/81 patients used paper/electronic data for their year-one service evaluation. Effectiveness: The automated, hybrid paper/electronic protocol optimized data management. Adoption: Rates of electronic patient-reported outcomes were higher in 2022-2023 than 2016-2017 (paper version). Completion rates for clinician-reported outcomes were highest at baseline (year-one). Implementation/maintenance: Barriers and facilitators, essential adaptations, and sustainable impacts were identified. Using electronic, measurement-based data collection accelerates feedback closer to real time and alignment with learning health system principles. Implementing the hybrid data collection platform at PEPP-Montreal provided valuable insights into using measurement-based care to inform quality of services. In the complex transition to a digital protocol within a learning health system, including engagement of key stakeholders, using the hybrid protocol was a necessary first step.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40086421,

title = {Sex and APOE4-specific links between cardiometabolic risk factors and white matter alterations in individuals with a family history of Alzheimer's disease},

author = {Stefanie A Tremblay and R Nathan Spreng and Alfie Wearn and Zaki Alasmar and Amir Pirhadi and Christine L Tardif and Mallar M Chakravarty and Sylvia Villeneuve and Ilana R Leppert and Felix Carbonell and Yasser Iturria Medina and Christopher J Steele and Claudine J Gauthier and },

doi = {10.1016/j.neurobiolaging.2025.03.003},

issn = {1558-1497},

year  = {2025},

date = {2025-06-01},

journal = {Neurobiol Aging},

volume = {150},

pages = {80--96},

abstract = {Early detection of pathological changes in Alzheimer's disease (AD) has garnered significant attention in the last few decades as interventions aiming to prevent progression will likely be most effective when initiated early. White matter (WM) alterations are among the earliest changes in AD, yet limited work has comprehensively characterized the effects of AD risk factors on WM. In older adults with a family history of AD, we investigated the sex-specific and APOE genotype-related relationships between WM microstructure and risk factors. Multiple MRI-derived metrics were integrated using a multivariate approach based on the Mahalanobis distance (D2). To uncover the specific biological underpinnings of these WM alterations, we then extracted the contribution of each MRI feature to D2 in significant clusters. Lastly, the links between WM D2 and cognition were explored. WM D2 in several regions was associated with high systolic blood pressure, BMI, and glycated hemoglobin, and low cholesterol, in both males and females. APOE4 + displayed a distinct risk pattern, with LDL-cholesterol having a detrimental effect only in carriers, and this pattern was linked to immediate memory performance. Myelination was the main mechanism underlying WM alterations. Our findings reveal that combined exposure to multiple cardiometabolic risk factors negatively impacts microstructural health, which may subsequently affect cognition. Notably, APOE4 carriers exhibited a different risk pattern, especially in the role of LDL, suggesting distinct underlying mechanisms in this group.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39120714,

title = {An intersectional perspective on the sociodemographic and clinical factors influencing the status of not in Education, Employment, or training (NEET) in patients with first-episode psychosis (FEP)},

author = {Jiaxuan Deng and Lisa Sarraf and Adèle Hotte-Meunier and Stéphanie El Asmar and Jai Shah and Ridha Joober and Ashok Malla and Srividya Iyer and Martin Lepage and Geneviève Sauvé},

doi = {10.1007/s00127-024-02732-z},

issn = {1433-9285},

year  = {2025},

date = {2025-06-01},

journal = {Soc Psychiatry Psychiatr Epidemiol},

volume = {60},

number = {6},

pages = {1367--1377},

abstract = {PURPOSE: High rates of Not in Education, Employment or Training (NEET) are seen in people with first episode of psychosis (FEP). Sociodemographic and clinical factors were reported to be associated with NEET status in FEP patients. This study follows Intersectionality to examine the independent and additive effects, and most importantly the intersections of sociodemographic and clinical variables concerning NEET status in FEP patients. It was hypothesized that NEET status in FEP patients would be described by the intersection between at least two predictor variables.nnMETHODS: Secondary analyses with chi-square tests, multiple logistic regression and Chi-squared Automatic Interaction Detection (CHAID) analyses were performed on 440 participants with FEP.nnRESULTS: Chi-square tests indicated that patient socioeconomic status and negative symptom severity were significantly and independently associated with their NEET status. Multiple logistic regression suggested additive effects of age (odds ratio = 1.61), patient socioeconomic status (odds ratio = 1.55) and negative symptom severity (odds ratio = 1.75) in predicting patients' NEET status. CHAID detected an intersection between patients' negative symptom severity and socioeconomic status in shaping their NEET status.nnCONCLUSION: This study explored how the NEET status of patients with FEP was explained not only by the separate effects of negative symptom severity and socioeconomic status but also by the unique intersections of their clinical and social identities. Findings indicated that functional outcomes of patients appear co-constructed by the intersections of multiple identities. Crucial clinical implications of complementing care for negative symptom severity with vocational resources to improve functional outcomes of patients are discussed.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40088050,

title = {Brain Imaging Phenotypes Associated with Polygenic Risk for Essential Tremor},

author = {Miranda Medeiros and Alexandre Pastor-Bernier and Houman Azizi and Zoe Schmilovich and Charles-Etienne Castonguay and Peter Savadjiev and Jean-Baptiste Poline and Etienne St-Onge and Fan Zhang and Lauren J O'Donnell and Ofer Pasternak and Yashar Zeighami and Patrick A Dion and Alain Dagher and Guy A Rouleau},

doi = {10.1002/mds.30167},

issn = {1531-8257},

year  = {2025},

date = {2025-06-01},

journal = {Mov Disord},

volume = {40},

number = {6},

pages = {1160--1171},

abstract = {Essential tremor (ET) is a common movement disorder with a strong genetic basis. Magnetic resonance imaging (MRI), particularly diffusion-weighted MRI (dMRI) and T1 MRI, have been used to identify brain abnormalities of ET patients. However, the mechanisms by which genetic risk affects the brain to render individuals vulnerable to ET remain unknown. We aimed to understand how ET manifests by identifying presymptomatic brain vulnerabilities driven by ET genetic risk. We probed the vulnerability of healthy people towards ET by investigating the association of morphometry, and white and grey matter dMRI with ET in polygenic risk scores (PRS) in roughly 30,000 individuals from the UK Biobank (UKB). Our results indicate significant effects of ET-PRS with mean diffusivity, fractional anisotropy, free water, radial diffusivity, and axial diffusivity in white matter tracts implicated in movement control. We found significant associations between ET-PRS and grey matter tissue microstructure, including the red nucleus, caudate, putamen, and motor thalamus. ET-PRS was associated with reduced grey matter volumes in several cortical and subcortical areas including the cerebellum. Identified anomalies included networks connected to surgical sites effective in ET treatment. Finally, in a secondary analysis, low PRS individuals compared with a small number of patients with ET (N = 49) in the UKB revealed many structural differences. Brain structural vulnerabilities in healthy people at risk of developing ET correspond to areas known to be involved in the pathology of ET. High genetic risk of ET seems to disrupt ET brain networks even in the absence of overt symptoms of ET. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39985309,

title = {Regional Cerebral Atrophy Contributes to Personalized Survival Prediction in Amyotrophic Lateral Sclerosis: A Multicentre, Machine Learning, Deformation-Based Morphometry Study},

author = {Isabelle Lajoie and  and Sanjay Kalra and Mahsa Dadar},

doi = {10.1002/ana.27196},

issn = {1531-8249},

year  = {2025},

date = {2025-06-01},

journal = {Ann Neurol},

volume = {97},

number = {6},

pages = {1144--1157},

abstract = {OBJECTIVE: Accurate personalized survival prediction in amyotrophic lateral sclerosis is essential for effective patient care planning. This study investigates whether grey and white matter changes measured by magnetic resonance imaging can improve individual survival predictions.nnMETHODS: We analyzed data from 178 patients with amyotrophic lateral sclerosis and 166 healthy controls in the Canadian Amyotrophic Lateral Sclerosis Neuroimaging Consortium study. A voxel-wise linear mixed-effects model assessed disease-related and survival-related atrophy detected through deformation-based morphometry, controlling for age, sex, and scanner variations. Additional linear mixed-effects models explored associations between regional imaging and clinical measurements, and their associations with time to the composite outcome of death, tracheostomy, or permanent assisted ventilation. We evaluated whether incorporating imaging features alongside clinical data could improve the performance of an individual survival distribution model.nnRESULTS: Deformation-based morphometry uncovered distinct voxel-wise atrophy patterns linked to disease progression and survival, with many of these regional atrophies significantly associated with clinical manifestations of the disease. By integrating regional imaging features with clinical data, we observed a substantial enhancement in the performance of survival models across key metrics. Our analysis identified specific brain regions, such as the corpus callosum, rostral middle frontal gyrus, and thalamus, where atrophy predicted an increased risk of mortality.nnINTERPRETATION: This study suggests that brain atrophy patterns measured by deformation-based morphometry provide valuable insights beyond clinical assessments for prognosis. It offers a more comprehensive approach to prognosis and highlights brain regions involved in disease progression and survival, potentially leading to a better understanding of amyotrophic lateral sclerosis. ANN NEUROL 2025;97:1144-1157.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40116508,

title = {Young children's preferences for their mothers: concurrent predictors and correlates},

author = {Gwendolyn Ngoh and Lit Wee Sim and Ai Peng Tan and Stella Tsotsi and Kerry Lee and Jerry K Y Chan and Michael J Meaney and Anne Rifkin-Graboi},

doi = {10.1080/14616734.2025.2467104},

issn = {1469-2988},

year  = {2025},

date = {2025-06-01},

journal = {Attach Hum Dev},

volume = {27},

number = {3},

pages = {350--367},

abstract = {A basic tenet of Attachment Theory describes a species-wide tendency to search out an attachment figure in times of distress. Expectations of support, or lack thereof, may provide a template for socioemotional functioning. This study investigated potential concurrent predictors (i.e. time spent with one's mother and parenting style) and socioemotional correlates of children's verbally expressed preferences for their mothers (i.e. maternal preference) during hypothetical attachment- and affiliation-related situations in 185 Southeast Asian children aged 3-6 years (95 boys). Though children in the current study were cared for by several caregivers, results here suggest they nevertheless prefer their mothers. Maternal time spent did not significantly predict preferences. However, authoritative parenting style scores did. Maternal preferences predicted higher child prosocial, but not problematic behavior. Implications for future work discerning the role of mothers in children's lives are discussed.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40566800,

title = {Biomarker changes associated with fornix deep brain stimulation in Alzheimer's disease},

author = {Jürgen Germann and Robert S C Amaral and Jennifer Tomaszczyk and Kazuaki Yamamoto and Gavin J B Elias and Flavia Venetucci Gouveia and Anna Vasilevskaya and Foad Taghdiri and Gabriel A Devenyi and Tejas Sankar and Jeannie-Marie Leoutsakos and Cynthia A Munro and Paul B Rosenberg and Constantine G Lyketsos and Esther S Oh and William S Anderson and Zoltan Mari and Lisa Fosdick and Kristen E Drake and Steven D Targum and Jo Cara Pendergrass and Anna Burke and Stephen Salloway and Wael F Asaad and Francisco A Ponce and Marwan Sabbagh and David A Wolk and Gordon Baltuch and Michael S Okun and Kelly D Foote and Peter Giacobbe and Mary Pat McAndrews and David F Tang-Wai and Gwenn S Smith and M Carmela Tartaglia and M Mallar Chakravarty and Andres M Lozano and },

doi = {10.1002/alz.70394},

issn = {1552-5279},

year  = {2025},

date = {2025-06-01},

journal = {Alzheimers Dement},

volume = {21},

number = {6},

pages = {e70394},

abstract = {INTRODUCTION: Deep brain stimulation of the fornix (fx-DBS) is being investigated for treatment of Alzheimer's disease (AD). The therapy aims at alleviating memory and cognitive circuit dysfunction. In preclinical models of AD, electrical stimulation of the memory circuit has demonstrated a possible disease-modifying potential. Here we examined changes resulting from fx-DBS in hippocampal atrophy and amyloid accumulation in AD patients with fx-DBS.nnMETHODS: Repeated magnetic resonance imaging and positron emission tomography (PET) images acquired over the course of 12 months were used to assess changes in hippocampal volume in 36 ADvance trial patients compared to 40 matched untreated AD patients from the Alzheimer's Disease Neuroimaging Initiative, and in 10 separate patients with repeated flutemetamol PET and cerebrospinal fluid (CSF) markers.nnRESULTS: We observed a reduction of hippocampal atrophy and amyloid beta (Aβ) PET binding, and an increase in the CSF Aβ/total-tau ratio in DBS patients.nnDISCUSSION: These findings highlight the potential of fornix deep brain stimulation to modify AD biomarkers and possibly progression in some patients.nnHIGHLIGHTS: Fornix deep brain stimulation (fx-DBS) is being investigated to treat Alzheimer's disease (AD). Results show that fx-DBS modifies imaging and cerebrospinal fluid (CSF) markers. It reduces hippocampal atrophy and increases the amyloid beta/total-tau CSF ratio. These findings highlight the potential of fx-DBS to modify AD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40550956,

title = {Fatty acid amide hydrolase in major depressive episodes: A [C]CURB positron emission tomography study},

author = {Dorsa Rafiei and Michelle De Pol and Jeffrey H Meyer and Kimberly Desmond and Ruth Ross and Isabelle Boileau and Jerry Warsh and Pablo Rusjan and Neil Vasdev and Ryan Aloysius and Lauren Gray and Nathan J Kolla},

doi = {10.1038/s41386-025-02150-y},

issn = {1740-634X},

year  = {2025},

date = {2025-06-01},

journal = {Neuropsychopharmacology},

abstract = {The role of the endocannabinoid system (ECS) in major depressive disorder (MDD) is under-investigated despite reports of increased activity and/or concentration of fatty acid amide hydrolase (FAAH), a key ECS enzyme, in fronto-limbic brain regions in some animal models of depressive behavior. We hypothesized that [C]CURB λk, an index of FAAH density, would be elevated in the prefrontal cortex, hippocampus, and anterior cingulate cortex in major depressive episodes of MDD compared to healthy controls. Fifteen unmedicated MDD participants and 15 age- and sex-matched healthy controls underwent [C]CURB positron emission tomography and FAAH genotyping. Psychological tests of depressive severity, apathy, and anxiety were administered and measurements were assessed as covariates in exploratory analyses. No significant group differences in [C]CURB λk were observed between MDD participants and controls (F = 0.32; p = 0.58). A mixed effects model revealed that Marin Apathy Evaluation Scale scores in the MDD group had a significant main effect on [C]CURB λk binding across the collective regions of medial prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex, ventral striatum, and midbrain (F = 6.75; p = 0.02). Depressive severity and anxiety did not have a significant relationship to [C]CURB λk binding. The relationship of greater fronto-limbic [C]CURB λk to greater apathy along with the metabolic role of FAAH in the ECS, the latter which supports maintaining feelings of interest, initiative, and motivation, has important implications for the pathophysiology of apathy in MDD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40523895,

title = {Relationship between grammar and schizophrenia: a systematic review and meta-analysis},

author = {Dalia Elleuch and Yinhan Chen and Qiang Luo and Lena Palaniyappan},

doi = {10.1038/s43856-025-00944-1},

issn = {2730-664X},

year  = {2025},

date = {2025-06-01},

journal = {Commun Med (Lond)},

volume = {5},

number = {1},

pages = {235},

abstract = {BACKGROUND: Schizophrenia significantly impairs everyday communication, affecting education and employment. Such communication difficulties may arise from deficits in syntax-understanding and generating grammatical structures. Research on syntactic impairments in schizophrenia is underpowered, with inconsistent findings, and it is unclear if deficits are specific to certain patient subgroups, regardless of symptom profiles, age, sex, or illness severity.nnMETHODS: A pre-registered (Open Science Framework: https://doi.org/10.17605/OSF.IO/7FZUC ) search using PubMed, Scopus, PsycINFO, and Web of Science databases up to May 1, 2024, for all studies investigating syntax comprehension and production in schizophrenia vs. healthy controls. Excluding studies on those <18 years of age and qualitative research, we extracted Cohen's d and log coefficient of variation ratio and used Bayesian meta-analysis across 6 domains: 2 in comprehension and 4 in production in patient-control comparisons. Study quality was evaluated using a modified Newcastle-Ottawa Scale, with moderators (age, sex, study quality, language) tested via meta-regression.nnRESULTS: We identify 86 relevant articles, of which 45 have sufficient data for meta-analysis (n = 2960 participants, 64.4% English, weighted mean age(sd) = 32.3(5.6)). Bayesian meta-analysis shows strong evidence of syntactic deficits in schizophrenia across all domains (d = 0.65-1.01, overall random-effects d = 0.86, 95% CrI [0.67-1.03]), with syntax comprehension being most affected, with weak publication bias. People with schizophrenia show increased variability in comprehension and production of long and complex utterances (lnCVR = 0.21, 95% CrI [0.07-0.36]), hinting at subgroups with differing performance.nnCONCLUSIONS: Robust impairments in grammatical comprehension and production in schizophrenia suggest opportunities for targeted interventions focusing on syntax, a rule-based feature amenable to cognitive, educational, and linguistic interventions.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40522287,

title = {Rate of brain aging associates with future executive function in Asian children and older adults},

author = {Susan F Cheng and Wan Lin Yue and Kwun Kei Ng and Xing Qian and Siwei Liu and Trevor W K Tan and Kim-Ngan Nguyen and Ruth L F Leong and Saima Hilal and Ching-Yu Cheng and Ai Peng Tan and Evelyn C Law and Peter D Gluckman and Christopher Li-Hsian Chen and Yap Seng Chong and Michael J Meaney and Michael W L Chee and B T Thomas Yeo and Juan Helen Zhou},

doi = {10.7554/eLife.97036},

issn = {2050-084X},

year  = {2025},

date = {2025-06-01},

journal = {Elife},

volume = {13},

abstract = {Brain age has emerged as a powerful tool to understand neuroanatomical aging and its link to health outcomes like cognition. However, there remains a lack of studies investigating the rate of brain aging and its relationship to cognition. Furthermore, most brain age models are trained and tested on cross-sectional data from primarily Caucasian, adult participants. It is thus unclear how well these models generalize to non-Caucasian participants, especially children. Here, we tested a previously published deep learning model on Singaporean elderly participants (55-88 years old) and children (4-11 years old). We found that the model directly generalized to the elderly participants, but model finetuning was necessary for children. After finetuning, we found that the rate of change in brain age gap was associated with future executive function performance in both elderly participants and children. We further found that lateral ventricles and frontal areas contributed to brain age prediction in elderly participants, while white matter and posterior brain regions were more important in predicting brain age of children. Taken together, our results suggest that there is potential for generalizing brain age models to diverse populations. Moreover, the longitudinal change in brain age gap reflects developing and aging processes in the brain, relating to future cognitive function.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40461469,

title = {Digital health technologies in the accelerating medicines Partnership® Schizophrenia Program},

author = {Johanna T W Wigman and Ann Ee Ching and Yoonho Chung and Habiballah Rahimi Eichi and Erlend Lane and Carsten Langholm and Aditya Vaidyam and Andrew Jin Soo Byun and Anastasia Haidar and Jessica Hartmann and Angela Nunez and Dominic Dwyer and Adibah Amani Nasarudin and Owen Borders and Isabelle Scott and Zailyn Tamayo and Priya Matneja and Kang-Ik Cho and Jean Addington and Luis K Alameda and Celso Arango and Nicholas J K Breitborde and Matthew R Broome and Kristin S Cadenhead and Monica E Calkins and Eric Yu Hai Chen and Jimmy Choi and Philippe Conus and Cheryl M Corcoran and Barbara A Cornblatt and Covadonga M Diaz-Caneja and Lauren M Ellman and Paolo Fusar-Poli and Pablo A Gaspar and Carla Gerber and Louise Birkedal Glenthøj and Leslie E Horton and Christy Lai Ming Hui and Joseph Kambeitz and Lana Kambeitz-Ilankovic and Matcheri S Keshavan and Sung-Wan Kim and Nikolaos Koutsouleris and Kerstin Langbein and Daniel Mamah and Daniel H Mathalon and Vijay A Mittal and Merete Nordentoft and Godfrey D Pearlson and Jesus Perez and Diana O Perkins and Albert R Powers and Jack Rogers and Fred W Sabb and Jason Schiffman and Jai L Shah and Steven M Silverstein and Stefan Smesny and Walid Yassin and William S Stone and Gregory P Strauss and Judy L Thompson and Rachel Upthegrove and Swapna Verma and Jijun Wang and Daniel H Wolf and Phillip Wolff and  and Laura M Rowland and Simon D'Alfonso and Ofer Pasternak and Sylvain Bouix and Patrick D McGorry and Rene S Kahn and John M Kane and Carrie E Bearden and Scott W Woods and Martha E Shenton and Barnaby Nelson and Justin T Baker and John Torous},

doi = {10.1038/s41537-025-00599-w},

issn = {2754-6993},

year  = {2025},

date = {2025-06-01},

journal = {Schizophrenia (Heidelb)},

volume = {11},

number = {1},

pages = {83},

abstract = {Although meta-analytic studies have shown that 25-33% of those at Clinical High Risk (CHR) for psychosis transition to a first episode of psychosis within three years, less is known about estimating the risk of transition at an individual level. Digital phenotyping offers a novel approach to explore the nature of CHR and may help to improve personalized risk prediction. Specifically, digital data enable detailed mapping of experiences, moods and behaviors during longer periods of time (e.g., weeks, months) and offer more insight into patterns over time at the individual level across their routine daily life. However, while novel digital health technologies open up many new avenues of research, they also come with specific challenges, including replicability of results and the adherence of participants. This paper outlines the design of the digital component of the Accelerating Medicines Partnership® Schizophrenia Program (AMP SCZ) project, a large international collaborative project that follows individuals at CHR for psychosis over a period of two years. The digital component comprises one-year smartphone-based digital phenotyping and actigraphy. Smartphone-based digital phenotyping includes 30-item short daily self-report surveys and voice diaries as well as passive data capture (geolocation, on/off screen state, and accelerometer). Actigraphy data are collected via an Axivity wristwatch. The aim of this paper is to describe the design and the three goals of the digital measures used in AMP SCZ to: (i) better understand the symptoms, real-life experiences, and behaviors of those at CHR for psychosis, (ii) improve the prediction of transition to psychosis and other health outcomes in this population based on digital phenotyping and, (iii) serve as an example for replicable and ethical research across geographically diverse regions and cultures. Accordingly, we describe the rationale, protocol and implementation of these digital components of the AMP SCZ project. **Link to video interview: https://vimeo.com/1060935583 *.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39545969,

title = {Mental health, risk behaviors, and social life factors in relation to adolescents' suicide ideation, plans and attempt},

author = {Stine Danielsen and Katrine Strandberg-Larsen and Massimiliano Orri and Merete Nordentoft and Annette Erlangsen and Trine Madsen},

doi = {10.1007/s00787-024-02616-2},

issn = {1435-165X},

year  = {2025},

date = {2025-06-01},

journal = {Eur Child Adolesc Psychiatry},

volume = {34},

number = {6},

pages = {1945--1958},

abstract = {OBJECTIVE: This study investigated differences in mental health and well-being, risk behaviors, and social life factors among adolescents who experienced different forms of suicidality.nnMETHODS: We examined 18-years-olds in the Danish National Birth Cohort (N = 47,852). Suicidality was defined with mutually exclusive categories ranging from no suicidality, self-reported suicide ideation, plans, and attempt as well as hospital-recorded suicide attempt. The proportion of adolescents with self-reported poor mental health and well-being, risk behaviors, and social life factors were compared across forms of suicidality. Sample weights were applied.nnRESULTS: Depressive symptoms were reported by 14% (95% CI 13%;14%) of girls with no suicidality, 44% (95% CI 43%;45%) of girls with suicide ideation, and 68% (95% CI 65%;72%) 66% (95% CI 60%;72%) of girls with self-reported suicide attempt or hospital-recorded suicide attempt respectively. Among boys, depressive symptoms were reported by 5% (95% CI 4%;5%) of those with no suicidality, 27% (95% CI 26%;28%) of those with suicide ideation, and 51% (95% CI 45%;57%) and 40% (95% CI 22%;58%) of those with self-reported suicide attempt or hospital-recorded suicide attempt respectively. Likewise, other aspects of poor mental health and well-being gradually increased relative with more severe forms of suicidality, while no notable differences were identified between adolescents with self-reported and hospital-recorded suicide attempt. Similar tendencies were observed for risk behaviors and social life factors.nnCONCLUSION: These findings suggest that adolescents with suicidality, including the large proportion with suicide ideation only, faces challenges across several parameters of mental health and well-being, risk behavior, and social life factors. This emphasizes the need for community-based interventions to identify and support the large group of adolescents experiencing both more and less severe forms of suicidality. Clinicians should prioritize comprehensive psychiatric intervention to address the complex needs of suicidal adolescents effectively.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40528492,

title = {The Music for Subanesthetic Infusions of Ketamine randomised clinical trial: ketamine as a psychedelic treatment for highly refractory depression},

author = {Kyle T Greenway and Nicolas Garel and Lê-Anh L Dinh-Williams and Julien Thibault Lévesque and Mendel Kaelen and Vincent Dagenais-Beaulé and Sara de la Salle and David Erritzoe and Karl Looper and Gustavo Turecki and Soham Rej and Séphane Richard-Devantoy},

doi = {10.1192/bjp.2025.102},

issn = {1472-1465},

year  = {2025},

date = {2025-06-01},

journal = {Br J Psychiatry},

pages = {1--9},

abstract = {BACKGROUND: Ketamine exerts potent but transient antidepressant effects in treatment-resistant depression (TRD). Combinations of ketamine and psychotherapy have attracted interest, but no trial has investigated a psychedelic model of ketamine-psychotherapy for TRD to our knowledge.nnAIMS: This secondary analysis of a randomised clinical trial (RCT) explores the therapeutic effects and experiential mechanisms of the Montreal Model of ketamine-psychotherapy for TRD, with or without music.nnMETHOD: A two-centre, single-blinded, RCT conducted in Montreal, Canada, between January 2021 and August 2022 (NCT04701866). Participants received ketamine-psychotherapy for TRD - six subanaesthetic infusions over 4 weeks and psychological support - with either music or matched non-music support during ketamine doses, as per random group assignments. The primary therapeutic outcome was the Montgomery-Åsberg Depression Rating Scale, assessed by blinded raters. Psychedelic-like experiences, evaluated by the Mystical Experience Questionnaire and Emotional Breakthrough Inventory, and their session-by-session relationships with depression were explored with multilevel, time-lagged covariate models with autoregressive residuals.nnRESULTS: Thirty-two participants with severe and highly comorbid TRD, including high rates of personality disorder and suicidality, received 181 ketamine infusions. Therapeutic outcomes and psychedelic experiences did not differ between music ( = 15) and non-music ( = 17) interventions. Both groups experienced significant reductions in clinician-rated and self-reported depression ( = 1.2 and  = 0.87, respectively;  < 0.001), anxiety ( = 0.8,  < 0.001) and suicidality ( = 0.4,  < 0.05) at 4 weeks, fully maintained at 8-week follow-up. Ketamine experiences were highly emotional and mystical. Converging analyses supported mystical-like ketamine experiences as mechanisms of its antidepressant effects.nnCONCLUSIONS: This trial found large and notably sustained benefits of ketamine-psychotherapy for severe TRD, with or without music, and psychedelic experiences of comparable intensity to those observed with psilocybin. Mystical-like experiences may particularly contribute to ketamine's immediate and persistent psychiatric benefits.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40543361,

title = {Norepinephrine system dysconnectivity in major depressive disorder: the effect of short term SSRI treatment},

author = {Shuting Chen and Jinqiang Zhang and Guowei Wu and Xuan Ouyang and Zhening Liu and Dongsheng Lv and Ziliang Han and Yonghui Xiang and Chen Tan and Can Xu and Lange Zheng and Xinran Xu and Lena Palaniyappan and Weidan Pu},

doi = {10.1016/j.euroneuro.2025.05.010},

issn = {1873-7862},

year  = {2025},

date = {2025-06-01},

journal = {Eur Neuropsychopharmacol},

volume = {97},

pages = {40--50},

abstract = {Despite the long history of norepinephrine hypothesis in depression, the neuropathology involving norepinephrine remains elusive. This study aims to map the whole-brain functional connectivity (FC) of the major norepinephrine nucleus locus coeruleus (LC) and further investigate the effect of escitalopram, an antidepressant with minimal direct norepinephrine effects, on the LCNE system in patients with major depressive disorder (MDD). Totally 253 MDD patients and 227 healthy controls (HCs) were recruited. The Philips-scanning dataset from Xiangya (52 patients and 88 HCs) served as the discovery sample, while the Siemens-scanning dataset from Xiangya (95 patients and 90 HCs) served as the across-scanner sample and the dataset from Inner Mongolia (88 patients and 53 HCs) as the across-center replication sample. Forty-eight patients entered a naturalistic observational trial of 8-weeks of escitalopram-only treatment. Bilateral LC were selected as regions of interest for FC analysis. Compared to HCs, patients exhibited decreased LCNE system connectivity with the multimodal association (dorsolateral/medial prefrontal) cortices and increased connectivity with the sensory/motor cortex. This imbalanced FC pattern replicated in two independent samples and consistently correlated with depressive symptom severity. The LCNE system dysconnectivity in MDD mapped with a significant overlap on the norepinephrine transporter distribution based on prior PET data. As expected, no significant changes of the LCNE connectivity occurred with 8-weeks of escitalopram treatment. We provide robust evidence for a striking sensory-multimodal imbalance in LCNE system connectivity across three independent samples, with a potential link to NE transporter chemoarchitecture, that is not alleviated by a serotonin selective antidepressant agent.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}