Publications

@article{pmid41809770,

title = {Sleeping without borders: Gaps in contextualizing sleep duration guidelines for adults in low-income countries},

author = {Reut Gruber and Jean-Philippe Chaput and Oliviero Bruni and Rosalie Barbeau},

doi = {10.1016/j.sleepx.2026.100176},

issn = {2590-1427},

year  = {2026},

date = {2026-12-01},

journal = {Sleep Med X},

volume = {11},

pages = {100176},

abstract = {BACKGROUND: Empirical data on adult sleep health are scarce in many low-income countries, despite the significant health risks associated with inadequate sleep. To help address this gap in low-income countries, the World Sleep Society's Global Sleep Health Taskforce recommends applying evidence from high-income settings - such as guidance from the American Academy of Sleep Medicine/Sleep Research Society AASM/SRS) and the National Sleep Foundation (NSF) to inform the development of sleep health policies and programs.nnOBJECTIVE: To evaluate the appropriateness of adapting existing consensus recommendations on healthy sleep duration for adults from the AASM/SRS and the NSF for use in low-income countries by applying World Health Organization (WHO) contextualization benchmarks.nnMETHODS: We reviewed AASM/SRS and NSF methods papers and assessed four WHO benchmarks: (1) consideration of low-income country priorities in question formulation and literature search; (2) inclusion of evidence from low-income countries; (3) involvement of stakeholders from low-income countries in consensus preparation; and (4) representation of low-income countries or relevant expertise in expert panels. Empirical studies cited in both statements were classified by country income level using World Bank 2025-2026 classifications. Chi-square tests compared distributions across income groups.nnRESULTS: Neither the AASM/SRS or NSF consensus process incorporated priorities, evidence, or representation from low-income countries. Of the empirical studies reviewed, 96% originated from high-income countries, 4% from upper-middle-income countries, and none from lower-middle-income countries (LMIC). No stakeholders or experts from low-income countries participated in guideline development. Both statements showed significant overrepresentation of high-income contexts (p < .001).nnCONCLUSIONS: Current sleep duration recommendations lack contextualization for low-income settings and do not meet WHO standards in this regard. Future guideline development should broaden evidence sources, engage local stakeholders, and apply participatory frameworks to ensure cultural relevance, equity, and practical implementation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41660498,

title = {Sleep without borders starts here: Principles and pathways for sleep health promotion},

author = {Reut Gruber and Winfried Randerath},

doi = {10.1016/j.sleepx.2025.100172},

issn = {2590-1427},

year  = {2026},

date = {2026-12-01},

journal = {Sleep Med X},

volume = {11},

pages = {100172},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40768120,

title = {Assessing Functional Limitations in Workers with a Common Mental Disorder or a Musculoskeletal Disorder: A Scoping Review of Questionnaires},

author = {Anaïs Lépine Lopez and Geneviève Sauvé and Marc Corbière},

doi = {10.1007/s10926-025-10310-6},

issn = {1573-3688},

year  = {2026},

date = {2026-09-01},

journal = {J Occup Rehabil},

volume = {36},

number = {3},

pages = {767--782},

abstract = {PURPOSE: Approximately, 80% of sick leave involve workers dealing with a common mental disorder (CMD) or a musculoskeletal disorder (MSD). Upon returning to work (RTW), these workers may encounter challenges, including functional limitations at work. However, assessing these limitations is complex. This study aims to map existing questionnaires that evaluate functional limitations in individuals with CMD or MSD.nnMETHODS: A scoping review was conducted following the methods of the Joanna Briggs Institute's (JBI) Scoping Reviews Methodology Group, utilizing five databases: ProQuest, EBSCO, Scopus, Cochrane, and PsycNET. Articles were included if they presented a questionnaire evaluating functional limitations or related concepts in individuals with CMD or MSD.nnRESULTS: A total of 541 articles were identified, with 6 articles selected after the screening process. The most frequently assessed dimensions in the selected questionnaires were physical (in 5 tools) and cognitive (in 3 tools). A thematic analysis was performed to develop a unified classification of dimensions and identify various types of functional limitations, addressing the inconsistent terminology across the questionnaires.nnCONCLUSION: Physical limitations seem to be more objective and easier to assess than psychological limitations. Future research should focus on psychological limitations to enhance understanding among healthcare professionals and individuals with CMD or MSD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41622438,

title = {Thalamic reticular nucleus in the pathophysiology of schizophrenia},

author = {Gonzalo Flores and David J Apam-Castillejos and Hannaford Edwards and Victor M Magdaleno-Madrigal and Juan Nacher and Hiram Tendilla-Beltrán and Lalit K Srivastava},

doi = {10.4103/NRR.NRR-D-25-00928},

issn = {1673-5374},

year  = {2026},

date = {2026-09-01},

journal = {Neural Regen Res},

volume = {21},

number = {9},

pages = {4045--4050},

abstract = {Mechanistic analyses on schizophrenia have traditionally focused on corticolimbic structures such as the prefrontal cortex, hippocampus, and amygdala, given their established roles in cognition. However, the thalamus, a critical hub that interconnects these regions, has garnered comparatively less attention. Of particular interest is the thalamic reticular nucleus, which plays a crucial role in cognition and sensory processing through its connections with the dorsomedial thalamic nucleus and the prefrontal cortex. A potential role of the thalamic reticular nucleus in schizophrenia has been suggested in a few reports; however, recent analyses have identified a specific link between the thalamic reticular nucleus and layer 5 neurons of the prefrontal cortex, a relationship highlighted by our group's earlier findings from 2012, which demonstrated that bilateral thalamic reticular nucleus lesions in adult rats caused neuronal atrophy in these cortical neurons. Building on this foundation, this manuscript explores the role of the thalamic reticular nucleus in schizophrenia neurobiology by reviewing its functional neuroanatomy, its integration within the corticolimbic system, and mechanisms of its potential involvement in the disease. This hypothesis is further developed by describing our novel findings from rats with neonatal ventral hippocampus lesion, widely considered a developmental model for schizophrenia. For the first time, we report dendritic spine pathology in thalamic reticular nucleus neurons, characterized by reduced spine density and a lower proportion of mushroom spines. Furthermore, we demonstrate a decrease in the density of parvalbumin-positive cells within the thalamic reticular nucleus in the neonatal ventral hippocampus lesion model. Together, these findings suggest significant alterations in the corticolimbic network and position the thalamic reticular nucleus as a complex yet promising mechanistic contributor to the neurobiology of schizophrenia.},

keywords = {},

pubstate = {published},

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}

@article{pmid42472313,

title = {Health service utilization by people with psychosis during Peru's mental health reform and the COVID-19 pandemic: a population-based study},

author = {Ruben Valle and Juan P Murillo and Peiyuan Huang and Cesar Gutierrez and Srividya N Iyer},

doi = {10.1016/j.lana.2026.101542},

issn = {2667-193X},

year  = {2026},

date = {2026-09-01},

journal = {Lancet Reg Health Am},

volume = {61},

pages = {101542},

abstract = {BACKGROUND: Individuals with psychosis face persistent barriers to care. Peru's recent mental health reform expanded services nationwide but coincided with the COVID-19 pandemic. We hypothesized that service utilization among individuals with psychosis would increase between 2018 and 2024, particularly in underserved regions.nnMETHODS: We analyzed outpatient morbidity data from the Peruvian National Superintendence of Health (2018-2024). Sex was available as binary male/female coding; gender identity and race/ethnicity data were not available. Service utilization was compared across three groups: psychosis, non-psychotic mental disorders, and general medical conditions. We examined changes in access (rate ratios, rate differences), the impact of the pandemic (interrupted time series), and decentralization trends (Poisson regression), separately for each disorder group.nnFINDINGS: In 2024 compared with 2018, monthly service utilization per 100,000 declined for psychosis (28.2 in 2018-19.2 in 2024; rate ratio 0.68), rose for non-psychotic mental disorders (225.2 in 2018-304.6 in 2024; 1.35), and slightly fell for general medical conditions (12,688.1 in 2018-12,370.4 in 2024; 0.97). The pandemic caused a comparable immediate drop in service utilization, with rates falling to 37.9%, 37.0%, and 35.3% of expected levels for the three groups in March 2020, followed by gradual monthly increases (psychosis 1.3%, non-psychotic mental disorders 2.6%, general medical conditions 2.2%). A shift from tertiary to primary and regional facilities was seen for both mental disorder groups, but greater utilization in underserved regions was observed only for non-psychotic mental disorders.nnINTERPRETATION: Despite nationwide expansion of mental health services, individuals with psychosis did not experience higher service use. The pandemic's impact was acute and enduring for this group. Findings underscore the need to examine reasons for this stagnation in service utilization and evaluate the acceptability and appropriateness of Peru's current service model for psychosis.nnFUNDING: Canadian Institutes of Health Research, Canada Research Chairs program.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid42247738,

title = {Low levels of organization and consistency in the home in middle childhood predicts cortisol levels and internalizing symptoms 12 years later among the offspring of parents with bipolar disorder},

author = {Mark A Ellenbogen and Lisa Serravalle and Sheilagh Hodgins and Claire-Dominique Walker and Elaine F Walker},

doi = {10.1016/j.psyneuen.2026.107904},

issn = {1873-3360},

year  = {2026},

date = {2026-09-01},

journal = {Psychoneuroendocrinology},

volume = {191},

pages = {107904},

abstract = {The offspring of parents with bipolar disorder (OBD) are at high risk for developing affective disorders. Low levels of organization and consistency in the home (parenting structure) is associated with increased behavioral problems and hypothalamic-pituitary-adrenal (HPA) reactivity in the OBD and thus may be an important developmental risk factor. We also examined whether the cortisol response following awakening (CAR) is increased in the OBD who developed an affective disorder relative to OBD with no affective disorder. The sample (19.3 ± 3.4 years) consisted of 68 OBD and 64 offspring (61 female) of parents with no affective disorder (controls). As predicted, offspring who developed an affective disorder had higher CAR than OBD who did not have an affective disorder (Cohen's d= 0.423) and controls (Cohen's d= 0.468). Bootstrapping serial mediation analyses revealed that parenting structure in middle childhood and the CAR in offspring significantly mediated the relationship between risk status and offspring depressive and anxiety symptoms 12 years later (CI:.01,.66). Low parenting structure in the OBD leads to changes in the HPA axis that increases the risk of developing symptoms of an affective disorder. Suboptimal childrearing may have enduring consequences on mental health outcomes in the OBD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42320794,

title = {Prenatal metabolic adversity reprograms insulin-responsive transcription in the developing nucleus accumbens},

author = {Bonnie Alberry and Barbara Barth and Aashita Batra and Marcio Bonesso Alves and Patricia Maidana Miguel and Nicholas O'Toole and Sachin Patel and Derek Lupinsky and Tie Yuan Zhang and Xianglan Wen and Danusa Mar Arcego and Daniela Pereira Laureano and Irina Pokhvisneva and Roberta Dalle Molle and Patricia Pelufo Silveira},

doi = {10.1016/j.molmet.2026.102405},

issn = {2212-8778},

year  = {2026},

date = {2026-08-01},

journal = {Mol Metab},

volume = {110},

pages = {102405},

abstract = {Prenatal metabolic adversity, including fetal growth restriction (FR), programs long-term alterations in systemic and neural insulin sensitivity, yet its impact on insulin signaling within reward-circuit plasticity across development remains poorly understood. Using a rodent model of gestational FR, we examined how early metabolic stress alters insulin regulation of mesolimbic reward circuits using in vivo chronoamperometry to measure nucleus accumbens (NAc) dopamine (DA) release during palatable food exposure, with and without peripheral insulin. We assessed longitudinal consumption behavior and conducted transcriptomic profiling (RNA-Seq) at birth (P0), weaning (P21), and adulthood (P90) following saline or insulin administration. FR blunted immediate NAc DA release in response to palatable food, a deficit specifically reversed by peripheral insulin, indicating altered insulin sensitivity of mesolimbic reward circuits. FR animals also display accelerated initial palatable food consumption. Transcriptomic analysis revealed that FR reprograms the NAc's molecular response to insulin. Across development and sex, only 2-9% of insulin-responsive genes overlap between FR and controls. FR generated condition-specific and frequently inverted transcriptional signatures, affecting genes linked to synaptic plasticity (Cplx3, Rab3b) and neurodevelopment (Ccn3). These findings demonstrate that prenatal adversity reconfigures the NAc by altering its molecular and neurochemical responsiveness to insulin. This developmental reprogramming reveals how early metabolic stress reshapes insulin sensitivity within reward circuitry, a mechanism that may contribute to both metabolic and psychiatric disease vulnerability.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42413520,

title = {Investing early in youth mental health: from promise to population evidence},

author = {Marie-Claude Geoffroy and Sylvana M Côté},

doi = {10.1016/S2215-0366(26)00199-9},

issn = {2215-0374},

year  = {2026},

date = {2026-08-01},

journal = {Lancet Psychiatry},

volume = {13},

number = {8},

pages = {629--631},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42413522,

title = {Return on investment of enhanced primary youth mental health services in a large Canadian urban centre: a retrospective cohort study},

author = {Jai L Shah and Nguyen Xuan Thanh and Shireen Surood and Surya Poudel and Liana Urichuk and Giuseppe D'Andrea and Eric Latimer and Neil Andersson and Patricia Boksa and Ridha Joober and Shalini Lal and Srividya N Iyer and Ashok Malla and Philip Jacobs and },

doi = {10.1016/S2215-0366(26)00165-3},

issn = {2215-0374},

year  = {2026},

date = {2026-08-01},

journal = {Lancet Psychiatry},

volume = {13},

number = {8},

pages = {657--668},

abstract = {BACKGROUND: Many youth mental health reforms aim to shift care away from acute, hospital, or institutional settings and into community-based services, but few such initiatives have been subject to economic evaluations. We aimed to examine service utilisation and the corresponding return on investment for individuals receiving care via an enhanced primary-care youth mental health service.nnMETHODS: We conducted a retrospective cohort study of an enhanced primary-care youth mental health service transformation in a major urban site of the pan-Canadian ACCESS Open Minds network, which provides assessment and interventions for all types and severities of mental health problems, with priorities co-designed by individuals with lived experience (young people, families, and carers). Administrative datasets were used to determine service utilisation and the associated costs, including programme implementation, for help-seeking youth aged 15-25 years with any mental health problem. A difference-in-differences approach compared outcomes pre-exposure with outcomes post-exposure to the ACCESS Open Minds service over 1 year, in relation to youth receiving a non-transformed service. Propensity score matching and sensitivity analyses ensured bias reduction and robustness of observations, respectively.nnFINDINGS: Between April 6, 2016, and Sept 30, 2019, 10 632 help-seeking youth (4821 [45·4%] males and 5801 [54·6%] females) were included. 1415 youths (mean age 20·1 years) received care from ACCESS Open Minds, and 9217 youths (19·3 years) received standard community mental health services. No ethnicity data were available in this administrative dataset. Compared with those receiving services in community mental health clinics, those receiving ACCESS Open Minds had more intensive service needs throughout the study period and had greater and statistically significant reductions in hospital admissions (CA$1961 savings); outpatient ($613 savings), specialist ($432 savings), and general practitioner visits ($47 savings); and public residential admissions ($1256 savings) per-person per-year. There were no significant differences in emergency department visits, the number of prescriptions dispensed, community mental health visits, or contracted residential admissions. Net cost reduction associated with ACCESS Open Minds was $4355 per-person per-year, with implementation costs of $448, representing a net benefit of $3907 (return on investment 9·7).nnINTERPRETATION: Consistent with principles of early intervention in mental health, ACCESS Open Minds implementation resulted in improved or equivalent outcomes but also shifted care towards community-based settings, with substantial net cost savings. These cost savings can be realised if novel services identify and treat not only new cases but also include those who were previously intensive users of standard services. The long-term return on investment of enhanced primary youth mental health models such as ACCESS Open Minds will likely rest on their commitment to including this population.nnFUNDING: Canadian Institutes of Health Research and the Graham Boeckh Foundation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42168643,

title = {Visual versus quantitative tau-PET Braak staging in Alzheimer's disease using [F]MK6240},

author = {Arthur C Macedo and Karine Provost and Jean-Paul Soucy and Arlette Haeger and Joseph Therriault and Lydia Trudel and Nesrine Rahmouni and Jaime Fernandez-Arias and Étienne Aumont and Aurélie Lebrun and Tevy Chan and Seyyed Ali Hosseini and Gleb Bezgin and Cécile Tissot and Stijn Servaes and Brandon Hall and Jenna Stevenson and Robert Hopewell and Chris Hung-Hsin Hsiao and Gallen Triana-Baltzer and Hartmuth C Kolb and Andréa L Benedet and Gassan Massarweh and Jesse Klostranec and Paolo Vitali and Tharick A Pascoal and Pedro Rosa-Neto},

doi = {10.1007/s00259-026-07886-3},

issn = {1619-7089},

year  = {2026},

date = {2026-08-01},

journal = {Eur J Nucl Med Mol Imaging},

volume = {53},

number = {10},

pages = {5644--5658},

abstract = {PURPOSE: The 2024 Alzheimer's Association Workgroup research framework designates tau proteinopathy (T) as a key element for Alzheimer's disease (AD) staging, but optimal staging approaches have yet to be determined. Here, we compared visual and quantitative tau-PET-based Braak staging as candidate strategies to implement T biological staging in vivo.nnMETHODS: We included 140 participants from the TRIAD cohort who underwent [⁸F]MK6240 tau-PET. Quantitative Braak staging (qBraak) was derived from regional SUVR thresholds, whereas visual Braak staging (vBraak) was independently performed by three nuclear medicine physicians using an adapted interpretation algorithm. Inter-rater and inter-method agreement were assessed using Cohen's and Fleiss' κ statistics. Associations with clinical severity, cortical thickness, plasma pTau217, and cortical tau extent were examined. Diagnostic performance for identifying amyloid-positive cognitively impaired individuals was evaluated.nnRESULTS: vBraak demonstrated substantial to nearly perfect inter-rater agreement (κ = 0.65-0.93). Agreement between vBraak and qBraak was moderate when stages were treated categorically (κ = 0.51), but substantial when their ordinal nature was considered (weighted κ up to 0.73). Both strategies showed comparable associations with clinical severity and neurodegeneration. vBraak was more sensitive to amyloid-β-positive cognitive impairment and identified intermediate-stage involvement at lower global tau extent. Visual-quantitative discordant cases were primarily attributable to off-target binding or spatially heterogeneous tau patterns.nnCONCLUSION: Both vBraak and qBraak staging provide complementary and largely concordant approaches for operationalizing T staging. Quantitative methods enable scalable, group-level analyses, whereas visual assessment remains essential for identifying atypical tau patterns and informing clinically relevant decision-making.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid41872521,

title = {A genome-wide investigation of depression among individuals with and without irritability},

author = {Julien St-Pierre and Jacky Jang and Corina Nagy and Laura Fiori and Gustavo Turecki and Josée Dupuis and Sahir Rai Bhatnagar and Massimiliano Orri},

doi = {10.1038/s41380-026-03548-w},

issn = {1476-5578},

year  = {2026},

date = {2026-08-01},

journal = {Mol Psychiatry},

volume = {31},

number = {8},

pages = {4323--4331},

abstract = {Individuals presenting with both depression and irritability may constitute a different group of individuals with respect to those presenting without irritability, but their biological differences remain unknown. We aimed to identify genetic variants associated with depression among individuals with and without irritability, highlight biological pathways, and test for genetic associations with other traits. We conducted a genome-wide association study (GWAS) using data from the UK Biobank (N = 487,409). We identified a group of individuals presenting with depression and reporting never having experienced irritability (depression without irritability, n = 35,857, 11.8%), and another with depression and reporting having experienced irritability (depression with irritability, n = 23,613, 8.1%) and compared them to controls with no depression or irritability (n = 268,012). The GWAS of depression without irritability identified 2 SNPs which reached genome-wide significance (P < 5×10; rs72795440 and rs1233494). The GWAS of depression with irritability (N = 292,485) identified 3 SNPs reaching genome-wide significance (rs2815748, rs102275, and rs7227069). When comparing SNPs between depression phenotypes, 15 SNPs had significantly different effect sizes. Patterns of genetic correlation with 44 complex traits were overall similar between the 2 depression phenotypes, with the highest genetic overlap observed with anxiety for depression without irritability (r = .77) and neuroticism for depression with irritability (r = .76). This study shed light into common and distinct biological factors characterizing depression among individuals with and without irritability and contribute to better understanding the genetic architecture of depression to potentially inform treatment and personalized medicine.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42441734,

title = {Canadian Network for Mood and Anxiety Treatments (CANMAT) and International College of Obsessive-Compulsive Spectrum Disorders (ICOCS) 2025 international guidelines for the management of patients with obsessive-compulsive disorder},

author = {Michael Van Ameringen and Naomi A Fineberg and Arun Ravindran and Paul D Arnold and Serge Beaulieu and Vlasios Brakoulias and Elisa Brietzke and Yekta Dowlati and Lynne M Drummond and Casara J Ferretti and Jamie D Feusner and Rafael C R Freire and Benicio N Frey and Sarah Gardiner and Daniel A Geller and Peter Giacobbe and Carolina Goldman Bergmann and Giacomo Grassi and Erica Greenberg and Eric Hollander and Paige Hopkinson and Sidney H Kennedy and Raymond W Lam and Christine Lochner and Joseph F McGuire and Sarah McQuay and Jose M Menchon and Roumen Milev and Luciano Minuzzi and Juliette Mojgani and Davis N Mpavaenda and Humberto Nicolini and Stefano Pallanti and Ilenia Pampaloni and Sagar V Parikh and Beth Patterson and Lakshmi Ravindran and Jemma Reid and Carolyn I Rodriguez and Zainab Samaan and Ayal Schaffer and Lukasz Smigielski and Valerie H Taylor and Smadar Valérie Tourjman and Peter van Roessel and Simone N Vigod and Susanne Walitza and Lakshmi N Yatham and Joseph Zohar and Morená Zugliani and Bernardo Maria Dell'Osso},

doi = {10.1016/j.jpsychires.2025.12.039},

issn = {1879-1379},

year  = {2026},

date = {2026-08-01},

journal = {J Psychiatr Res},

volume = {199},

pages = {404--488},

abstract = {BACKGROUND: As a joint effort by the Canadian Network for Mood and Anxiety Treatments (CANMAT) and the International College of Obsessive-Compulsive Spectrum Disorders (ICOCS), these treatment guidelines provide an up-to-date synthesis of published literature on the efficacy, safety, and tolerability of the range of interventions available for the management of obsessive-compulsive disorder (OCD) across the lifespan. The primary goal is to provide clear, easy to use recommendations for practicing clinicians.nnMETHODS: A global group of OCD experts were divided into panels to develop specific sections based on internal group discussions and the evidence extracted from systematic literature searches. CANMAT-defined Levels of Evidence, as well as level of clinical support were used to inform Lines of Treatment and final treatment recommendations. Drafts were revised based on feedback from individuals with lived experience, expert peer review, and a defined expert consensus process.nnRESULTS: These OCD Guidelines include seven sections spanning foundations of management and diagnosis, psychological, pharmacological, and neuro-modulation treatment modalities, treatment resistance, children and adolescents, special populations and future directions. Recommendations are summarized in tables for ease of reference and caveats and limitations of the current evidence are discussed.nnCONCLUSIONS: The CANMAT/ICOCS 2025 OCD International Guidelines synthesize the evidence on the efficacy, safety, and tolerability of the range of interventions available for the management of OCD. It is anticipated that these new OCD guidelines will enable psychiatrists and other clinicians to provide systematic, evidence-based care for their patients with OCD across the lifespan.},

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pubstate = {published},

tppubtype = {article}

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@article{pmid41370074,

title = {Family-Focused Recommendations in Canadian Guidelines for Early Intervention Services for Psychosis: A Systematic Review: Recommandations axées sur la famille dans les Lignes directrices canadiennes relatives aux services d'intervention précoce en cas de psychose : Une revue systématique},

author = {Helen Martin and Ruben Valle and Nicole Pawliuk and Srividya N Iyer},

doi = {10.1177/07067437251393981},

issn = {1497-0015},

year  = {2026},

date = {2026-08-01},

journal = {Can J Psychiatry},

volume = {71},

number = {8},

pages = {593--605},

abstract = {BackgroundDespite well-known benefits of family involvement and interventions, gaps remain in their implementation in early intervention for psychosis. Guidelines have been developed for early psychosis services to bridge evidence-implementation gaps. Little attention has been paid to their nature, quality and recommendations regarding family involvement and interventions. We aimed to identify, describe, and appraise family-focused recommendations in Canadian early psychosis guidelines.MethodsWe conducted a systematic review (PROSPERO#CR042020208974), including Canadian guidelines/standards for first-episode psychosis/early intervention in psychosis, or for psychosis/schizophrenia with a section on first-episode psychosis/early intervention for psychosis. The search was conducted in Google and Google Advanced of 58 websites (April 2024). From each document, bibliographic information and family-focused recommendations were extracted. All family-focused recommendations were subject to content analysis and mapped against a patient and family engagement framework. All guidelines were appraised using Appraisal of Guidelines Research & Evaluation-Recommendation EXcellence (AGREE-REX), assessing rigor and implementability. Family-focused recommendations were rated on three AGREE-REX items. Findings were narratively synthesized.ResultsSeven documents were included, with five provincial early psychosis guidelines and two Canada-wide schizophrenia-spectrum guidelines. 96 family-focused recommendations were extracted covering 21 themes (19 appeared in ≤4 guidelines; two (family psychoeducation; involving families in treatment-planning) in five guidelines). No guidelines had recommendations regarding families in inpatient care; only two guidelines had recommendations for navigating consent vis-à-vis family involvement. 77.4% of recommendations were about direct care; 22.5% about involving families in organizational design/governance; and none about policymaking involvement. AGREE-REX ratings for relevant outcomes and local applicability were lower for family-focused recommendations than overall guidelines. Most guidelines fared poorly in eliciting families' values/preferences.ConclusionFew family-focused recommendations featured consistently across early psychosis guidelines. There was little guidance on navigating barriers to family involvement. Our analysis revealed critical gaps, including in viewing families as partners in treatment decision-making and services/policy design. Future guidelines must integrate stakeholders' values/preferences and guidance on real-world implementation.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid42456683,

title = {Survival estimates and their predictors in genetic frontotemporal dementia: an international, retrospective, cohort study},

author = {Arabella Bouzigues and Mario Grassi and Valentina Cantoni and Enrico Premi and Sonia Bellini and Giuliano Binetti and Giancarlo Logroscino and Lucy L Russell and Eve Ferry-Bolder and Phoebe H Foster 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 Giuseppe Di Fede and Isabel Santana and Alexander Gerhard and Tobias Langheinrich and Johannes Levin and Benedetta Nacmias and Markus Otto and Maxime Bertoux and Thibaud Lebouvier and Simon Ducharme and Christopher Butler and Isabelle le Ber and Rose Bruffaerts and Eino Solje and Mika Kinnunen and Johanna Krüger and Elizabeth Finger and Maria Carmela Tartaglia and Mario Masellis and James B Rowe and Matthis Synofzik and Fermin Moreno and Roberta Ghidoni and Raffaella Migliaccio and Jonathan D Rohrer and Barbara Borroni and },

doi = {10.1016/S1474-4422(26)00197-3},

issn = {1474-4465},

year  = {2026},

date = {2026-08-01},

journal = {Lancet Neurol},

volume = {25},

number = {8},

pages = {731--740},

abstract = {BACKGROUND: What drives the heterogeneity of survival estimates in genetic frontotemporal dementia is unknown. We sought to understand the natural history and predictors of disease trajectory, which are crucial not only for effective care but also for the design of therapeutic clinical trials and efficacy evaluation.nnMETHODS: In this international, cohort study, we used the Kaplan-Meier method to retrospectively assess survival estimates in patients enrolled in the GENFI cohort, which included 32 research sites located in Belgium, Canada, Finland, France, Germany, Italy, the Netherlands, Portugal, Spain, Sweden, and the UK, and comprised participants carrying a causal C9orf72 expansion or a causal mutation in GRN or MAPT genes. Survival was calculated as the time from symptom onset to time of death or censoring date; median survival estimate for all patients was the primary endpoint. Cox proportional hazards models were used to identify predictors of survival, which were subsequently externally validated in an independent cohort. We further designed a structural equation model to assess the relationships between predictors, applying a least absolute shrinkage and selection operator method.nnFINDINGS: Of 278 participants of the GENFI cohort included in this study, 160 (58%) were men and 118 (42%) were women. 162 died during follow-up (58%) and 116 were still alive (42%) on June 1, 2024, the chosen censoring date. 138 participants carried a C9orf72 expansion, 94 carried a GRN mutation, and 46 a MAPT mutation. 179 participants were diagnosed with behavioural variant frontotemporal dementia, 46 with primary progressive aphasia, and 31 with frontotemporal dementia-amyotrophic lateral sclerosis. 22 participants had other diagnoses. The median survival estimate for all patients with genetic frontotemporal dementia was 6·94 years (95% CI 6·59-7·80) from symptom onset. The median survival estimate for patients with GRN mutations was 6·63 years (6·08-7·98), for patients with a C9orf72 expansion was 7·04 years (6·45-8·77), and for patients with MAPT mutations was 8·56 years (7·06-13·50). Older age at onset, shorter disease duration from onset to enrolment in the GENFI study, clinical presentation (ie, frontotemporal dementia-amyotrophic lateral sclerosis), domain of first symptom (ie, motor or language onset), and geographical area of residency (ie, central and southern Europe) were associated with poorer prognosis. Genetic group did not directly affect survival estimates; rather its effect was mediated by age at onset and clinical phenotype. We computed a genetic frontotemporal dementia survival risk index, which can be used at an individual patient level.nnINTERPRETATION: Our results highlight that motor impairment in addition to cognitive and behavioural symptoms should be considered when estimating prognosis in genetic frontotemporal dementia. Individual risk scores might be of help for patient stratification in future therapeutic trials, although refinement and prospective validation are now needed.nnFUNDING: Italian Ministry of Health (Ricerca Corrente), Fondation Philippe Chatrier, and Fondation Vaincre Alzheimer.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41935644,

title = {Human APOB-expressing mice translate molecular phenotypes across the Alzheimer's disease spectrum},

author = {Gabriel Aumont-Rodrigue and Alexandre Poirier and Cynthia Picard and Judes Poirier and },

doi = {10.1016/j.bbi.2026.106575},

issn = {1090-2139},

year  = {2026},

date = {2026-08-01},

journal = {Brain Behav Immun},

volume = {136},

pages = {106575},

abstract = {BACKGROUND: Apolipoprotein B (APOB), a structural component of low-density lipoproteins (LDL), has historically been associated with peripheral lipid transport and cardiovascular disease. Recent studies have revealed a link between APOB and Alzheimer's disease (AD), with increased cerebrospinal fluid (CSF) APOB levels correlating with tau pathology. Although APOB is known to be locally expressed in the brain, albeit at very low levels, its function in the central nervous system and contribution to neurodegenerative processes remains poorly understood. To investigate the effects of chronic APOB overexpression on brain molecular homeostasis, we used a transgenic mouse model expressing human APOB-100 and integrated findings with human cohort data to assess its functional relevance to AD pathology.nnMETHODS: Human APOB transgenic (hAPOB) and wild-type mice were aged to 6 and 12 months. Frontal cortices were analyzed using RNA sequencing and mass spectrometry-based proteomics. Differentially expressed genes and proteins were analyzed via pathway enrichment and cell type deconvolution. Findings were contrasted to post-mortem proteomic alterations observed in brain tissue (ROSMAP) and in the CSF (ADNI).nnRESULTS: hAPOB overexpression in mice induced a robust and persistent upregulation of innate immune genes, particularly those associated with type I interferon responses (Irf7, Ifit1, Oas2), in both young and old transgenic mice. Reduced microglial and endothelial cell signatures were observed through cell type deconvolution, which suggests immune activation without proliferation and possible blood-brain barrier damage. Proteomic analyses showed differentially expressed proteins associated with oxidative stress and dendritic remodeling. Proteins dysregulated in mice-such as CTSD, CRK, and SULT4A1-also showed altered expression in AD human brain and CSF. Remarkably, these proteins are dysregulated in the opposite direction in humans than in mice, unveiling a complex downstream regulation of APOB overexpression.nnCONCLUSION: Chronic hAPOB overexpression drives sustained neuroinflammatory and oxidative responses, potentially mimicking viral-like immune activation in the brain. The proteins dysregulated in hAPOB transgenic mice brains were also dysregulated in humans on opposite side of the APOB level spectrum. Nevertheless, this result shows a consistency across species on hAPOB-driven downstream effects. Some of these proteins were also shown to associate with key features of AD pathology, namely Aβ, Tau and pTau. Our findings support a novel role for APOB in modulating brain immune homeostasis and neurodegenerative processes, offering a mechanistic link between vascular risk and Alzheimer's disease.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41935185,

title = {Local chemoarchitecture explains widespread lower cortical thickness associated with clinical high risk for psychosis},

author = {Xi Yang and Ingrid Agartz and Ole Andreassen and Peter Bachman and Inmaculada Baeza and Cali Bartholomeusz and Stefan Borgwardt and Sunah Choi and Tiziano Colibazzi and Rebecca Cooper and Cheryl Corcoran and Camilo de la Fuente-Sandoval and Bjørn Ebdrup and Adriana Fortea and Birte Yding Glenthøj and Louise Birkedal Glenthøj and Shalaila Haas and Holly Hamilton and Rebecca Hayes and Ying He and Karsten Heekeren and Wenche Ten Velden Hegelstad and Christine Hooker and Michael Kaess and Kiyoto Kasai and Naoyuki Katagiri and Minah Kim and Jochen Kindler and Shinsuke Koike and Tina Kristensen and Jun Soo Kwon and Stephen Lawrie and Jimmy Lee and Ashleigh Lin and Rachel Loewy and Daniel Mathalon and Patrick McGorry and Chantal Michel and Paul Møller and Takahiro Nemoto and Marta Pena and Jayachandra Raghava and Francisco Reyes-Madrigal and Luis Rivera-Chávez and Wulf Rössler and Daiki Sasabayashi and Ulrich Schall and Andre Schmidt and Lukasz Smigielski and Mikkel Sørensen and Gisela Sugranyes and Tsutomu Takahashi and Christian Tamnes and Jinsong Tang and Anastasia Theodoridou and Jordina Tor and Peter Uhlhaas and Tor Værnes and Esther Via and Sophia Vinogradov and James Waltz and Lars Westlye and Stephen Wood and Hidenori Yamasue and Alison Yung and Juan Zhou and Paolo Fusar-Poli and Romina Mizrahi and Vanessa Cropley and Paul Thompson and Therese van Amelsvoort and Maria Jalbrzikowski and Benjamin Becker and David E J Linden and Dennis Hernaus and },

doi = {10.1038/s41380-026-03586-4},

issn = {1476-5578},

year  = {2026},

date = {2026-08-01},

journal = {Mol Psychiatry},

volume = {31},

number = {8},

pages = {4716--4726},

abstract = {The Clinical High Risk (CHR) state for psychosis is consistently associated with widespread cortical thinning. However, the underlying mechanisms driving this neuroanatomical phenotype remain poorly understood. Here, we integrated the ENIGMA CHR Working Group's large pooled dataset (N = 1782 CHR, N = 1333 healthy controls) with an open-source PET molecular atlas to identify, for the first time, potential neurochemical drivers of cortical thinning associated with psychosis risk, transition, and its core symptoms. Using multilinear model analysis, we show that local chemoarchitecture significantly explains CT differences associated with CHR case-control status, the severity of negative symptoms, and future psychosis transition after excluding medication confounds. PET-based maps of dopamine, GABA, glutamate, serotonin, and norepinephrine consistently emerged as the strongest predictors of lower CT in CHR and psychosis transition (total dominance range: 62-69% and 58-87%, respectively), with contributions of monoamine systems being especially sensitive to medication exposure (8-23% change in dominance range). Negative symptom-associated cortical thinning was best explained by PET-based maps of dopamine, histamine, serotonin and opioid systems (total dominance range: 60-81%), with contributions of histamine being sensitive to medication exposure (9-19% change in dominance range). Combined, these results uniquely identify specific neurochemical systems - particularly monoaminergic, glutamatergic, and GABAergic pathways - as key molecular mechanisms associated with cortical thinning in people at high risk of developing psychosis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42479994,

title = {Association Between Plasma GFAP and Medial Temporal Atrophy and Cognition in Amyloid-Negative Cerebrovascular Disease},

author = {Markley Silva Oliveira-Junior and Matheus Scarpatto Rodrigues and Livia Amaral and Guilherme Povala and Andreia Rocha and Marina Scop Medeiros and Sarah Abbas and João Pedro Ferrari-Souza and Pampa Saha and Firoza Z Lussier and Pamela C L Ferreira and Guilherme Bauer-Negrini and Carolina Soares and Hyun Woong Roh and Eduardo Rigon Zimmer and Thomas Karikari and Helmet Karim and Pedro Rosa-Neto and Chang Hyung Hong and Dana Tudorascu and Sang Joon Son and Bruna Bellaver and Tharick Pascoal},

doi = {10.1212/WNL.0000000000218336},

issn = {1526-632X},

year  = {2026},

date = {2026-08-01},

journal = {Neurology},

volume = {107},

number = {3},

pages = {e218336},

abstract = {BACKGROUND AND OBJECTIVES: Plasma glial fibrillary acidic protein (GFAP), a marker of astrocyte reactivity, is elevated across multiple neurodegenerative conditions, including Alzheimer disease. However, its role in neurodegeneration and cognitive decline driven by cerebrovascular pathology, independent of β-amyloid (Aβ) copathology, remains poorly characterized. We investigated whether plasma GFAP is associated with medial temporal atrophy and cognition across a spectrum of cerebrovascular burden in Aβ-negative cognitively impaired individuals.nnMETHODS: In this cross-sectional multicenter study, Aβ PET-negative cognitively impaired participants were recruited from South Korean memory clinics. Plasma GFAP was measured using ultrasensitive Simoa assays. White matter hyperintensity burden was graded using the Fazekas scale and stratified into low (LVP: Fazekas 1) and high (HVP: Fazekas 2-3) cerebrovascular burden groups. Medial temporal gray matter density was assessed using voxel-based morphometry, and hippocampal and amygdalar volumes were derived from T1-weighted MRI adjusted for intracranial volume. Linear regression, interaction, and bootstrap mediation models were used to assess associations among GFAP, brain structure, and cognition.nnRESULTS: A total of 324 participants were included (LVP n = 203; HVP n = 121; median age 73 years [interquartile range 66-78]; 67.9% female). Compared with LVP, HVP participants were older (75 vs 71 years;  < 0.0001), had lower Mini-Mental State Examination (MMSE) scores (22.7 vs 24.5;  = 0.005), and higher plasma GFAP (136.7 vs 112.1 pg/mL;  = 0.001). Higher GFAP was associated with lower medial temporal gray matter density in HVP (β = -0.311;  = 0.001) but not LVP (β = -0.012;  = 0.858), with a significant GFAP-vascular burden interaction (β = -0.309;  = 0.008). In HVP, higher GFAP was associated with smaller hippocampal (β = -0.179;  = 0.044) and amygdalar volumes (β = -0.169;  = 0.049) and lower MMSE (β = -0.194;  = 0.039). Medial temporal atrophy statistically explained the GFAP-MMSE association (indirect β = -0.071, 95% CI -0.140 to -0.010;  = 0.016). Vascular comorbidities (diabetes, dyslipidemia, hypertension) did not modify the GFAP-cognition association.nnDISCUSSION: In Aβ-negative cognitively impaired individuals with high cerebrovascular burden, elevated plasma GFAP is associated with medial temporal atrophy and cognitive decline, suggesting GFAP may capture astrocyte-reactivity relevant to vascular cognitive impairment beyond amyloid pathology. These cross-sectional findings require confirmation in longitudinal and ethnically diverse cohorts.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41922795,

title = {Sex-specific neurodevelopmental pathways to depressive symptoms},

author = {Shi Yu Chan and Pei Huang and Zhen Ming Ngoh and Joanne S M Chia and Janice Lee and Aisleen M A Manahan and Jasmine S M Chuah and Marielle V Fortier and Fabian Yap and Yap-Seng Chong and Peter Gluckman and Johan Eriksson and Michael J Meaney and Ai Peng Tan},

doi = {10.1038/s41380-026-03576-6},

issn = {1476-5578},

year  = {2026},

date = {2026-08-01},

journal = {Mol Psychiatry},

volume = {31},

number = {8},

pages = {4563--4575},

abstract = {While sex differences in the prevalence of depression are consistently observed in adolescence, sex-specific endophenotypes associated with depression appear earlier in childhood. Our study examined whether neurodevelopmental changes in childhood associated with depressive symptoms in adolescence show sex-specificity. Longitudinal multi-modal neuroimaging data were collected at ages 4.5, 6.0, and 7.5 years. Neurodevelopment was measured by structure-function coupling (SC-FC), the correlation between structural and functional connectivity, derived for 114 cortical regions and averaged across the whole cortex. Depressive symptoms were self-reported at age 13 years with the Child Depression Inventory (CDI), Youth Self Report (YSR), and Multidimensional Anxiety Scale for Children. Partial least squares correlation was used to identify latent variables that maximized covariance between the 28 CDI items and 114 cortical regions. Females reported significantly higher depressive symptoms than males at age 13 years (N = 636, p < 0.001). Whole cortex SC-FC showed sex-specific trajectories across childhood (N = 549, 917 scans). Females showed a steeper decrease in SC-FC relative to males in the pre-school phase (ages 4.5 to 6.0, p = 0.019) but not during mid-childhood (ages 6.0 to 7.5, p = 0.340). For both childhood phases (Pre-school: N = 97, Mid-childhood: N = 162), sex-specific models better explained the data than full cohort ("All") models. Items/regions with significant contributions to their respective latent variables were distinct in males and females and between childhood phases. Sex-specific cortical changes improved regression models predicting YSR Depressive Problems. We provide evidence for sex-specific childhood neurodevelopmental pathways to depressive symptoms in adolescence that could guide the timing for more effective intervention programs.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41980683,

title = {Choroid plexus inflammation in bipolar disorder},

author = {Dario Figueroa Velez and Reza Rahimian and Christine Hehnly and Jordan C Benson and Isabella Sacharczyk and Gustavo Turecki and Naguib Mechawar and Maria K Lehtinen},

doi = {10.1016/j.bbi.2026.106598},

issn = {1090-2139},

year  = {2026},

date = {2026-08-01},

journal = {Brain Behav Immun},

volume = {136},

pages = {106598},

abstract = {Inflammation has emerged as a prominent feature of bipolar disorder (BD) pathophysiology, drawing attention to brain barriers known to regulate immune-brain interactions. While perturbation of the blood-brain barrier has been reported in BD, the blood-cerebrospinal fluid (CSF) barrier formed largely by the choroid plexus (ChP) remains underexamined. To address this gap in knowledge, we used a multiplex array to measure cytokine protein abundance in postmortem ChP tissue from individuals with BD and unaffected controls, revealing elevated levels of CCL2 and SPP1, factors associated with monocyte and macrophage recruitment and activation. In contrast, expression of cytokines involved in tissue homeostasis, trophic support, and immune signaling, including OSM, IGF-1, CX3CL1, TGFB3, GDNF, LIF, BDNF, SCF, and FGFs, was reduced. Several cytokines, including CCL2 and PLGF, exhibited condition-specific divergent age trajectories. Bulk RNA sequencing of the same cohort revealed a modest set of differentially expressed genes, including transcripts associated with oxidative stress, mitochondrial function, and immune regulation that were upregulated in BD. Notably, the BD CSF biomarker NELL2 was downregulated in the ChP. Gene set enrichment analysis highlighted activation of inflammatory and cellular stress pathways, as well as reduced expression of junction-related gene programs. These findings suggest a shift in ChP function in BD characterized by increased pro-inflammatory signaling and reduced trophic and barrier-supportive activity. Together, these data identify the ChP as an active site of immune dysregulation in BD and support the broader notion of brain barrier dysfunction in mood disorder pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42504398,

title = {Phenotypic Behavioural Effects of Genetic Deletion of the Vesicular Glutamate Transporter 3 in 5-Hydroxytryptamine Neurons},

author = {L Sophie Gullino and Nida Chabbah and Spatika Jayaram and Raquel Pinacho and Salah El Mestikawy and Stéphanie Daumas and David M Bannerman and Trevor Sharp},

doi = {10.1111/gbb.70063},

issn = {1601-183X},

year  = {2026},

date = {2026-08-01},

journal = {Genes Brain Behav},

volume = {25},

number = {4},

pages = {e70063},

abstract = {A major subpopulation of 5-hydroxytryptamine (5-HT) neurons expresses the vesicular glutamate transporter 3 (VGLUT3) allowing the co-release of glutamate. Previous evidence has implicated VGLUT3 in 5-HT neurons in mechanisms of anxiety and reward. Here we examined mice with a genetic loss of VGLUT3 targeted to 5-HT neurons (VGLUT3 cKO) and littermate controls in a battery of behavioural tests, including paradigms assessing levels of anxiety and learning with appetitive rewards. Compared to littermate controls, VGLUT3 cKO mice displayed no evidence of altered anxiety-like behaviour in the elevated plus maze, light/dark box, marble burying and social interaction tests. However, VGLUT3 cKO mice showed reduced preference for low (but not high) sucrose-containing solution and reduced correct responses in an appetitively motivated spatial reference memory task. Similarly, in an appetitively motivated operant task, VGLUT3 cKO mice displayed evidence of reduced responding to cues associated with reward. These effects appeared specific in that VGLUT3 cKO mice did not differ from controls in terms of home cage food consumption, performance in a spatial novelty preference test, as well as contextual and cued fear memory tests. These findings support a role for VGLUT3 in 5-HT neurons in some aspects of learning, here in association with learning for reward, although not anxiety-like behaviour.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40974052,

title = {Age of Onset, Brain Controllability, and Working Memory Performance in First-Episode Schizophrenia},

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

doi = {10.1093/schbul/sbaf156},

issn = {1745-1701},

year  = {2026},

date = {2026-07-01},

journal = {Schizophr Bull},

volume = {52},

number = {4},

abstract = {BACKGROUND AND HYPOTHESIS: The onset-age of schizophrenia introduces considerable heterogeneity in cognitive functions such as working memory (WM) among patients. One of the key properties of the brain that varies with age-related development is the network-level controllability of brain state transitions. We tested the effect of onset-age on brain controllability to evaluate its impact on WM deficits in schizophrenia.nnSTUDY DESIGN: We examined the average and modal controllability of the brain connectome in 85 first-episode early-onset schizophrenia (EOS), 62 younger healthy controls (yHC), 71 first-episode adult-onset schizophrenia (AOS), and 85 older healthy controls (oHC) during N-back tasks. We first detected the regions with illness and onset-age interaction in a whole-brain search, and then conducted a correlation analysis with WM performance and clinical characteristics, followed by an out-of-sample gene annotation analysis.nnSTUDY RESULTS: We detected the illness*onset-age interaction in the sensorimotor network, auditory network, and subcortical network for average controllability and the default mode network, visual network, and salience network for modal controllability (p-fdr < 0.05). The interaction effects in the visual and subcortical networks primarily resulted from the AOS vs. oHC differences; the effects in the default mode network resulted from EOS vs. yHC differences. We observed no significant correlation between controllability with cognitive performance or clinical characteristics. The affected regions had preferential expression of genes relevant to synaptic signaling and neurodegenerative processes (p-fdr < 0.05).nnCONCLUSION: Onset-age introduces considerable heterogeneity in the controllability over brain state transition during WM tasks among patients with schizophrenia.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40971561,

title = {Subcategories of the Clinical High-Risk State for Psychosis and Their Relationship to a Full First-Episode Psychosis Sample: An Exploratory Analysis of Longitudinal Outcomes},

author = {Olivier Renaud-Charest and Vincent Paquin and Jean-Gabriel Daneault and Ashok K Malla and Ridha Joober and Srividya N Iyer and Martin Lepage and Jai L Shah},

doi = {10.1093/schbul/sbaf155},

issn = {1745-1701},

year  = {2026},

date = {2026-07-01},

journal = {Schizophr Bull},

volume = {52},

number = {4},

abstract = {BACKGROUND AND HYPOTHESIS: Subcategories of the Clinical High-Risk state for psychosis (CHR-P) have been associated with differential risk for transition to first-episode psychosis (FEP), but their relevance for longer term FEP outcomes remains unclear. We aimed to determine the prevalence of 2 CHR-P subcategories - attenuated psychotic symptoms (APS) and brief intermittent psychotic symptoms (BIPS) - in a full sample of FEP patients, along with their association with outcome trajectories following psychosis onset.nnSTUDY DESIGN: Participants were recruited from an early intervention service and followed over 2 years, with repeated measures of psychotic symptoms, affective symptoms, and functioning. Pre-onset symptoms were assessed using follow-back methods to reconstruct subgroups and their prevalence within the sample. Linear mixed models were applied to examine associations between putative CHR-P subcategories and longitudinal outcomes.nnSTUDY RESULTS: Of 319 patients, 240 (75.24%) experienced subthreshold psychotic symptoms indicative of a CHR-P state; of these, 51 (21.25%) had potential BIPS (either alone or with APS) and 189 (78.75%) potential APS only. There were no mean differences in scores for psychotic symptoms, affective symptoms, or functioning between subgroups. However, there was a slower improvement in Global Assessment of Functioning (GAF) scores in the putative APS subgroup, which converged with the putative BIPS subgroup by year 2.nnCONCLUSIONS: Putative CHR-P subcategories of APS and BIPS exhibited similar outcome trajectories beyond psychosis onset, except for a possibly slower functional recovery in the putative APS subgroup. Longer term studies across stages of illness are needed to better understand the prognostic utility of these identifiers after FEP.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41861248,

title = {Glucocorticoid Receptor-Regulated Gene Networks and Mental Health},

author = {Michael J Meaney and Elisabeth B Binder},

doi = {10.1146/annurev-neuro-102124-031826},

issn = {1545-4126},

year  = {2026},

date = {2026-07-01},

journal = {Annu Rev Neurosci},

volume = {49},

number = {1},

pages = {105--123},

abstract = {Stressors, including those occurring in early development, predict an increased risk for psychopathology. The challenge is that of defining causal pathways that connect stressful conditions to specific health outcomes and then leveraging this knowledge toward treatments. This review focuses on glucocorticoids (GCs), the end products of stressor-induced hypothalamic-pituitary-adrenal axis activity, and reviews evidence, including recent multiomics analyses, regarding their role in mental health. We outline the challenges in translating this knowledge into effective treatments and recent evidence for the potential of gene network analyses to identify molecular pathways linking stress to psychopathology. A detailed examination of GC activity through the glucocorticoid receptor is presented as an example of the complexities involved in achieving this research objective and paths to novel interventions through gene network analyses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42094851,

title = {Comprehensive analysis of cytokines in depression: independent data from patient plasma and post-mortem ventromedial prefrontal cortex},

author = {Reza Rahimian and Jonas Hagenberg and Claudia Belliveau and Rebecca Chen and Stephanie Théberge and Gohar Fakhfouri and Marina Wakid and Elisabeth Binder and Gustavo Turecki and Janine Knauer-Arloth and Naguib Mechawar},

doi = {10.1016/j.bbih.2026.101245},

issn = {2666-3546},

year  = {2026},

date = {2026-07-01},

journal = {Brain Behav Immun Health},

volume = {54},

pages = {101245},

abstract = {Preclinical and clinical evidence has implicated inflammation in the pathophysiology of depression. Abnormal cytokine levels in blood, cerebrospinal fluid, and post-mortem brain samples have been associated with depression. To our knowledge, however, a comprehensive analysis of cytokine protein levels in brain samples from patients with depression has yet to be conducted in major components of the limbic system such as the ventromedial prefrontal cortex (vmPFC). This region plays a crucial role in depression, impacting cognitive control, emotional regulation, and executive functions. In the current exploratory study, we performed a comprehensive profiling of 72 cytokines, chemokines and growth factors in well-characterized vmPFC samples from 34 depressed suicides and 14 matched sudden-death controls. A human antibody array (RayBio®, chemiluminescent detection) was used to measure all markers. In depressed suicide samples, no significant increase in any cytokine, chemokine or growth factor was detected compared to controls. In comparison, in an independent cohort we measured the levels of 43 inflammatory markers in plasma samples from 141 depressed living subjects and 36 controls using the Mesoscale Discovery V-plex assay. Our analyses indicated no significant difference in the levels of pro- or anti-inflammatory markers in the plasma of cases vs controls. We also conducted a detailed morphological analysis of Iba1-immunostained microglia in vmPFC gray matter samples from 28 depressed suicides and 13 healthy controls. The distributions of the various morphological phenotypes assessed were similar between groups, suggesting that microglia/macrophages do not display signs of morphological changes in the vmPFC of depressed suicides. Taken together, these complementary experiments do not provide evidence of depression-associated neuroinflammatory changes in the vmPFC, at least in the samples analyzed.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41950833,

title = {Experience of continuity of care mitigates poorer infant temperament for women reporting elevated hardship during pregnancy: Birth In The Time of COVID (BITTOC) study},

author = {Mia A McLean and Belinda Lequertier and Suzanne King and Sue Kildea and Hazel Keedle and Hannah G Dahlen},

doi = {10.1016/j.midw.2026.104779},

issn = {1532-3099},

year  = {2026},

date = {2026-07-01},

journal = {Midwifery},

volume = {158},

pages = {104779},

abstract = {PROBLEM: It is unknown whether unborn infants exposed to their mothers' uncontrollable stressful life events could benefit from the continuity of their mothers' prenatal carer.nnBACKGROUND: Maternal stress in pregnancy predicts poorer child outcomes. Continuity of care improves maternal mental health.nnAIM: Determine whether continuity of care moderates association between prenatal maternal stress due to COVID-19 and infant negative emotionality at age 6 months.nnMETHODS: Australian women, pregnant during the pandemic, completed a survey detailing their level of continuity of maternity care, pandemic-related difficulties (objective hardship), cognitive appraisal of, and subjective distress related to, COVID-19. Six months post-birth, they reported on their mental health, COVID-19 related stress and their infants' negative emotionality (n = 903).nnFINDINGS: Hierarchical multiple regression analysis showed that higher prenatal pandemic-related subjective distress was associated with greater infant negative emotionality. Interaction analyses determined that, for women exposed to higher levels of objective hardship in pregnancy, the more they experienced continuity of carer, the lower their child's negative emotionality at age 6 months. This relationship was not evident for dyads exposed to lower objective hardship. However, actual model of maternity care did not moderate the relationships between COVID-19-related prenatal maternal stress and infant negative emotionality. All models accounted for 6-month maternal COVID-19 objective hardship and subjective stress as well as depressive symptoms.nnDISCUSSION: We found that the protective effect of experienced continuity of care, small but potentially consequential, was most evident among women exposed to high COVID-19-related hardship. This finding supports the roll-out of maternity care models that foster relational continuity for at-risk pregnant women with additional medical and psychological needs.nnCONCLUSION: For women most exposed to uncontrollable stressful events, such as pandemic-related restrictions and threat, their experience of high continuity of care may predict long-term benefits for their infant's temperament.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42166041,

title = {Prenatal maternal stress is associated with alterations in the structural integrity of the hypothalamic-pituitary-gonadal axis 20 years later: Project Ice Storm},

author = {Sherri Lee Jones and Chloe Anastassiadis and Matthieu Dupuis and Guillaume Elgbeili and Francois-Pierre Marcoux and James Gazetas and Gabriel A Devenyi and Jamie Near and David P Laplante and Jens C Pruessner and Suzanne King},

doi = {10.1093/humrep/deag067},

issn = {1460-2350},

year  = {2026},

date = {2026-07-01},

journal = {Hum Reprod},

volume = {41},

number = {7},

pages = {1156--1172},

abstract = {STUDY QUESTION: Is prenatal maternal stress (PNMS) in humans associated with alterations in the sexually differentiated reproductive axis structures in the offspring?nnSUMMARY ANSWER: PNMS, experienced by pregnant mothers exposed to a natural disaster in 1998, was associated with structural changes in hypothalamic-pituitary-axis (HPG) structures of 18.5-year-old offspring.nnWHAT IS KNOWN ALREADY: In a human prospective study, PNMS was associated with higher childhood BMI, which in turn predicted earlier menarche. Epidemiological studies have shown that maternal life event stress is associated with changes in gonadal morphology and function.nnSTUDY DESIGN, SIZE, DURATION: A prospective study of mothers exposed to a severe ice storm in 1998 (N = 224) collected measures of PNMS (objective hardship and subjective distress). Offspring reproductive structures were assessed in early adulthood.nnPARTICIPANTS/MATERIALS, SETTING, METHODS: PNMS-exposed offspring (ICE; n = 39, 21 F, 18 M) and a control group (n = 31, 14 F, 17 M; born in 1997) were assessed at age 18.5 years. Participants underwent MRI. Using a novel approach, the structural integrity of the entire HPG axis was assessed using gold-standard manual delineation from their MRI scans. Ovarian antral follicles (2-10 mm) were also counted from MRI images. Salivary estradiol and testosterone were measured with ELISA. Data were analyzed with ANOVA and multiple regression.nnMAIN RESULTS AND THE ROLE OF CHANCE: The expected sex difference in hypothalamic volume (M > F) was detected in controls. Within ICE, the sex difference was observed at low, but not at high, levels of PNMS (objective and subjective). Greater objective hardship was associated with smaller hypothalamic volume in men. Similarly, pituitary volume was smaller in ICE men compared to control men. Within ICE, greater objective hardship was associated with smaller left testicular volume. Finally, compared to controls, the left ovary had more antral follicles and tended to be larger in ICE women. The group differences and associations between PNMS and HPG morphology were generally medium to large.nnLIMITATIONS, REASONS FOR CAUTION: The relatively small sample size may have limited our ability to detect small differences and to test interactions with gestational timing of prenatal stress exposure. In addition, the majority of women were taking oral contraceptives, and thus results must be interpreted with caution.nnWIDER IMPLICATIONS OF THE FINDINGS: PNMS from a natural disaster may lead to functional changes in the human reproductive axis in adulthood.nnSTUDY FUNDING/COMPETING INTEREST(S): Funding was provided by a grant from the Canadian Institutes of Health Research (CIHR, FRN 125892; to S.K., D.P.L., and J.C.P., and CIHR MOP 125892 to co-investigators S.K. S.L.J. was funded by a postdoctoral fellowship provided by the Fonds de Québec-Santé (FRQ-S). The funding sources were not involved in the collection, analyses, or interpretation of the data, or writing of the report. The authors have no competing interests to declare.nnTRIAL REGISTRATION NUMBER: N/A.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41936158,

title = {Care trajectories of Quebec patients with substance-related disorders within five years before death},

author = {Marie-Josée Fleury and Zhirong Cao and Guy Grenier},

doi = {10.1016/j.psychres.2026.117130},

issn = {1872-7123},

year  = {2026},

date = {2026-07-01},

journal = {Psychiatry Res},

volume = {361},

pages = {117130},

abstract = {AIMS: This study identifies care trajectories five years before death of 1468 patients with substance-related disorders (SRDs), associated with the patients' social and clinical characteristics, quality of care received, and causes of death.nnMETHODS: Care trajectories integrated outpatient SRD, mental health (MH) and physical health care, and acute care. Group-based multi-trajectory modeling identified service use patterns in three-month intervals across the five years preceding death. Multinomial logistic regression assessed associations between trajectory membership, patient characteristics, quality of care received, and causes of death.nnRESULTS: Four distinct trajectories emerged: "Low service users" (Profile 1, 34 % of sample, the reference group), "High physical health service users" (Profile 2, 30 %), "High but decreasing SRD service users" (Profile 3, 15 %), and "High but decreasing mental disorder (MD) service users, high users of other services" (Profile 4, 21 %). Profile 1 comprised mostly younger men with better health but poor continuity and regularity of care. Profile 3 patients had the most severe conditions, received the most intensive care, but had more accidental/intentional deaths than Profile 1. Profile 2 included older patients with severe chronic physical illnesses, injection drug use, and more emergency department users than Profile 1. Profile 4 had older patients reporting more MDs, suicidal behaviors, lower functioning, and greater use of specialized MH care.nnCONCLUSION: Service use was low overall and remained low even near death. Physical health care was the most used, followed by acute care. SRD and MH care declined before death across all profiles. Tailored interventions for each profile are suggested.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41935494,

title = {The association between body mass index and treatment outcomes in major depressive disorder: a CAN-BIND-1 study},

author = {Helena K Kim and Brett D M Jones and Margaret K Hahn and Sri Mahavir Agarwal and Faranak Farzan and Benicio N Frey and Sidney H Kennedy and Jane A Foster and Raymond W Lam and Roumen Milev and Daniel J Müller and Sagar V Parikh and Claudio N Soares and Valerie H Taylor and Gustavo Turecki and Rudolf Uher and Stefan Kloiber},

doi = {10.1016/j.jpsychires.2026.03.036},

issn = {1879-1379},

year  = {2026},

date = {2026-07-01},

journal = {J Psychiatr Res},

volume = {198},

pages = {252--256},

abstract = {Being overweight is commonly observed in patients with major depressive disorder (MDD). However, the relationship between body weight and treatment outcomes in MDD is less clear. In this context, we examined the association between BMI and treatment outcomes in patients treated with escitalopram with and without adjunctive aripiprazole. We tested this association using data from the Canadian Biomarker Integration Network in Depression-1 (CAN-BIND-1). The sample consisted of 180 participants who were treated with escitalopram for 8 weeks, followed by 8 more weeks of treatment with escitalopram alone (for responders) or escitalopram plus aripiprazole (for non-responders). Punishment/reward sensitivity and physical activity were also explored. Logistic regression analysis was used to examine the association between BMI, being overweight, and treatment response or remission after 8 or 16 weeks of treatment. BMI, being overweight, physical activity, behavioral inhibition, and behavioral activation were not associated with treatment outcomes. We also reviewed the recent literature on BMI, obesity, and antidepressant treatment outcomes, which showed mixed findings. Our results, which showed a lack of association between BMI and treatment outcomes, add to this complexity of the relationship between body weight and treatment outcomes in MDD. Larger studies with more diverse samples are needed to validate these results.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42537246,

title = {Routine follow-up care patterns after psychiatric hospital discharge and associations with rehospitalization and mortality: a longitudinal cohort study using latent class analysis},

author = {Pamela Obegu and Xiangfei Meng and Marie-Josée Fleury},

doi = {10.1016/j.genhosppsych.2026.07.011},

issn = {1873-7714},

year  = {2026},

date = {2026-07-01},

journal = {Gen Hosp Psychiatry},

volume = {102},

pages = {115--122},

abstract = {OBJECTIVE: The risk of psychiatric readmission and death is high in the year after discharge. Existing posthospitalization interventions show modest and sometimes inconsistent average effects, suggesting that optimizing routine follow-up care may require identifying clinically meaningful heterogeneity in routine care practice. This study aims to identify latent subgroups of follow-up care patterns during the 12 months after psychiatric discharge and examine their associations with patient characteristics, rehospitalization, and all-cause mortality.nnMETHODS: Using provincial linkable health administrative databases, we investigated a cohort of 3467 patients discharged after psychiatric hospitalization. Latent class analysis was used to identify subgroup memberships of follow-up care. Multivariable analyses estimated subgroups' associations with patient social and clinical correlates, and survival analyses estimated subgroups' associations with rehospitalization and all-cause mortality.nnRESULTS: Five distinct subgroups of follow-up care patterns were identified, including low to high quality of care, diversified care and high access to primary care, with two subgroups having frequent emergency (ED) use. Serious mental disorders and prior hospitalizations were concentrated in the high follow-up care subgroups, where rehospitalization hazards were significantly elevated and approached one-third. Mortality did not differ across subgroups.nnCONCLUSION: Follow-up care after psychiatric discharge is heterogeneous, reflecting patients' clinical risk profiles and outpatient contexts. Rehospitalization was driven primarily by clinical severity, while frequent ED use signalled unmet follow-up care needs, demonstrating two distinct post-discharge dynamics with different implications for quality monitoring and service improvement. These findings support subgroup-informed post-discharge optimization and may help explain the average modest effects of transitional interventions observed in prior research. Both carry direct relevance for policy and practice.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42532033,

title = {A cortical-hypothalamic neural circuit for compulsive eating in mice},

author = {Yi Ning Leow and Esra Senol and Xing Qian and Xiaoyu Wang and Aditya Nair and Olivia Khoo and Xiaoning Liu and Yi-Fei Li and Menghan Wang and Shivangi Sharma and Yi Zhang and Xiaodong Han and Marielle V Fortier and Michael J Meaney and Yap Seng Chong and Anna Magdalena Fogel and Keri McCrickerd and Ai Peng Tan and Fang Wang and Ti-Fei Yuan and Juan Helen Zhou and Hasan Mohammad and Yu Fu},

doi = {10.1016/j.neuron.2026.07.005},

issn = {1097-4199},

year  = {2026},

date = {2026-07-01},

journal = {Neuron},

abstract = {Binge-eating disorder (BED) is the most common eating disorder and is strongly associated with obesity. The medial prefrontal cortex (mPFC) has been implicated in compulsive behavior and is known to project to multiple hypothalamic cell types implicated in maladaptive feeding. How the mPFC engages hypothalamic networks and whether such interactions are relevant for human disease remain unknown. Here, using a binge-eating-induced compulsive eating (BiCOM) paradigm in mice, we demonstrate that rostral zona incerta γ-aminobutyric acid (GABAergic) neurons (GABA) drive compulsive eating. Manipulating either GABA neurons or their mPFC inputs bidirectionally modulated compulsive eating. In vivo imaging showed that BiCOM modified mPFC neural dynamics, creating persistent attractor states driven by, and with sustained selectivity for, palatable food. Moreover, human fMRI showed that mPFC-rostral zona incerta (rZI) connectivity correlated with body weight and binge eating. Together, these results identify a cortical-hypothalamic mechanism for compulsive eating in mice and highlight potential targets for intervention in BED and obesity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42526764,

title = {Emergency department use trajectories over a 10-year period among patients with substance-related disorders},

author = {Marie-Josée Fleury and Zhirong Cao and Guy Grenier and Xiangfei Meng},

doi = {10.1016/j.josat.2026.210081},

issn = {2949-8759},

year  = {2026},

date = {2026-07-01},

journal = {J Subst Use Addict Treat},

volume = {191},

pages = {210081},

abstract = {OBJECTIVES: Overutilization of the emergency department (ED) is costly and often reflects unmet needs and suboptimal care, raising concerns when patients rely on the ED persistently over many years. Long-term ED use trajectories for patients with substance-related disorders (SRDs) have never been investigated. This study aimed to identify ED use trajectories over a 10-year period and examine associations with patients' sociodemographic and clinical characteristics, quality-of-care indicators, and subsequent adverse outcomes.nnMETHODS: A cohort of 9642 patients with long-standing SRDs was examined using Québec (Canada) medical records (1996-2022). Group-Based Trajectory Modeling identified 10-year ED use trajectories. Multinomial logistic regression assessed associations between trajectories and covariates, while Cox models examined links to subsequent adverse outcomes (suicidal behavior, hospitalization, death).nnRESULTS: Four ED use trajectories were identified: Trajectory 1 ("Low ED users," 50% of cohort), Trajectory 2 ("Increasing ED users," 20%), Trajectory 3 ("Sinusoidal ED users," 20%), and Trajectory 4 ("Very frequent ED users," 10%). Half of the cohort showed frequent ED use (≥3 visits/year), including 10% who were very frequent users (≥8 visits/year), underscoring substantial unmet needs. ED use frequency was strongly linked to social and health conditions-most favorable in Trajectory 1, who were mostly men, and markedly worse in Trajectories 4, 2, and 3. Adverse outcomes were also strongly associated with poorer social and health conditions and lower treatment motivation, even though Trajectories 4, 2, and 3 received more healthcare services.nnCONCLUSION: Findings indicate that the healthcare system is not adequately structured to meet the needs of patients with severe multimorbidity involving SRDs, mental disorders, chronic physical illnesses, and social instability, contributing to care quality insufficiently meeting the complex needs of Trajectories 2-4. Tailored interventions may be warranted, including Integrated Treatment for Dual Disorders and Assertive Community Treatment for Trajectories 2 and 4, and Intensive Case Management, Recovery Management Checkups, or mobile health technologies for Trajectory 3. Across Trajectories 2-4, enhanced motivational interventions, social support, reduced stigma, optimized medication management, peer-helper programs, and stronger ED-outpatient collaboration remain essential. Improving services for patients with frequent ED use-particularly those in Trajectory 4 with recurrent very frequent use-should be prioritized to reduce costs, optimize service use, and support recovery.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42522874,

title = {Pathways to schizophrenia: Divergent effects of childhood trauma and polygenic risk on cognition and subcortical dynamics},

author = {Danqing Huang and Yicheng Long and Zhening Liu and Wenjian Tan and Xiawei Liu and Yunzhi Pan and Feiwen Wang and Lena Palaniyappan},

doi = {10.1192/j.eurpsy.2026.12246},

issn = {1778-3585},

year  = {2026},

date = {2026-07-01},

journal = {Eur Psychiatry},

pages = {1--39},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42521894,

title = {Long‑Term Gambling Disorder Care Trajectories and Associated Patient Characteristics and Quality of Care},

author = {Marie-Josée Fleury and Zhirong Cao and Guy Grenier and Sylvia Kairouz and Francine Ferland},

doi = {10.1007/s10899-026-10540-0},

issn = {1573-3602},

year  = {2026},

date = {2026-07-01},

journal = {J Gambl Stud},

abstract = {Given the limited evidence on the long‑term course of gambling disorder (GD), this study identified GD care trajectories, estimated GD duration, and examined their associations with patient and gambling characteristics and quality of care. A cohort of 2,154 patients with GD was examined using Quebec's administrative health records. We generated 13‑year GD care trajectories (2009-2022) using group‑based trajectory modeling. Multinomial logistic regression assessed the influence of sociodemographic, clinical, and gambling characteristics and quality‑of‑care indicators on trajectory membership. Four care trajectories were identified: Trajectory 1 (Transient GD, 34%), Trajectory 2 (Low‑intensity GD, 32%), Trajectory 3 (High initial, decreasing GD, 18%), and Trajectory 4 (Chronic GD, 16%). Two thirds of patients had GD records for an average of 1-2 years (Trajectories 1-2); GD persisted for 4 years in Trajectory 3 and 8 years in Trajectory 4. Compared with Trajectory 1, Trajectories 4 and 3 included patients more likely to be in their 50s and at higher risk of presenting severe clinical conditions, whereas Trajectory 2 patients were likelier to be younger, more socioeconomically deprived, and at greater risk of having a criminal history and co‑occurring alcohol‑ and drug‑related disorders. Patients in Trajectories 4 and 3 were more likely to receive GD‑specific treatments than those in Trajectories 1 and especially 2; however, Trajectories 2, 3, and 4 were at higher risk of showing lower treatment motivation. Trajectories 4 and 2 were also more likely to use non‑GD health services. Patients with long‑standing GD would benefit from enhanced follow‑up and crisis‑intervention strategies. Overall, improved detection across non‑GD care settings is needed to increase help‑seeking and support this vulnerable population.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42520805,

title = {Parent-of-origin effects in Alzheimer's liability dissociate neurocognitive and cardiovascular traits in at-risk individuals},

author = {Chloé Savignac and Frédéric St-Onge and Sylvia Villeneuve and AmanPreet Badhwar and Sarah A Gagliano Taliun and Sali Farhan and Maiya Geddes and Yasser Iturria Medina and Judes Poirier and R Nathan Spreng and Danilo Bzdok and },

doi = {10.1016/j.xcrm.2026.102943},

issn = {2666-3791},

year  = {2026},

date = {2026-07-01},

journal = {Cell Rep Med},

pages = {102943},

abstract = {Alzheimer's disease (AD) has a higher prevalence in women than men and is more frequently inherited from mothers than fathers. Yet, while neuroimaging and biomarker studies link maternal family history to stronger AD-related alterations, epidemiological studies suggest that paternal history confers comparable or even greater risk. Here, we leverage the deeply profiled PREVENT-AD cohort to derive three intermediate phenotypes of AD susceptibility. Drawing on nearly 1,000 individual study visits, we quantify how these intermediate phenotypes vary as a function of maternal versus paternal AD lineage. We show that lineage-specific differentiation, including both maternal and paternal biases, is reflected in the brain structure and phenome of adult children of AD patients. Cognitive and cardiovascular risk markers, together with associated genetic variants, show the strongest differentiation along the parental-lineage spectrum of disease susceptibility relative to other correlates of AD burden. Our cross-generational analysis ultimately delineates multidimensional parent-of-origin effects in AD genealogy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42410482,

title = {Shared and Distinct Clinical Features in Treatment-Seeking Adults With Avoidant/Restrictive Food Intake Disorder or Anorexia Nervosa Subtypes},

author = {Vittoria Trolio and Linda Booij and Samantha Ginsberg and Sarah E Racine and Howard Steiger},

doi = {10.1002/eat.70167},

issn = {1098-108X},

year  = {2026},

date = {2026-07-01},

journal = {Int J Eat Disord},

abstract = {OBJECTIVE: Available studies comparing clinical features in treatment-seeking adults with avoidant/restrictive food intake disorder (ARFID) to anorexia nervosa (AN) often do not distinguish between AN-restricting (AN-R) and AN-binge-eating/purging (AN-B/P) subtypes, rely on retrospective ARFID diagnoses, and include unequal group sizes. Across relatively balanced study groups, we compared eating disorder symptoms, concurrent psychiatric symptoms, and Big Five personality traits in treatment-seeking adults with ARFID, AN-R, or AN-B/P to identify unique and shared features.nnMETHODS: Participants were adults (29 ARFID, 39 AN-R, 45 AN-B/P) diagnosed via semi-structured clinical interviews at the start of outpatient treatment. Data were analyzed with general linear models.nnRESULTS: On measures of shape-/weight-centered eating pathology and depression, individuals with ARFID scored lower than did those with AN-R (ps < 0.05) or AN-B/P (ps < 0.001). On measures of anxiety, individuals with ARFID scored lower than did those with AN-B/P (p < 0.001) but not AN-R (p = 0.075). Compared with AN groups, the ARFID group had less total emotion-regulation difficulties (p < 0.001). There were no group differences on Big Five personality traits (p = 0.173), including neuroticism.nnDISCUSSION: Treatment-seeking adults with ARFID reported less shape-/weight-centered eating pathology, depression, anxiety, and emotion-regulation difficulties than did individuals with AN but did not differ on endorsement of Big Five personality traits. Findings suggest that individuals with ARFID display less pronounced psychopathology on assessed domains than do those with AN and highlight potential directions for future ARFID research.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42418951,

title = {An appraisal of practice guidelines for early intervention services for psychosis: Using AGREE II (Appraisal of Guidelines for Research and Evaluation) to enhance the quality and trustworthiness of guidelines in the future},

author = {Manuela Ferrari and Nicole Pawliuk and Jai Shah and Amal Abdel-Baki and Phil Tibbo and Donald Addington and Marc-André Roy and Ridha Joober and Kevin MacDonald and Srividya N Iyer},

doi = {10.1016/j.schres.2026.06.005},

issn = {1573-2509},

year  = {2026},

date = {2026-07-01},

journal = {Schizophr Res},

volume = {295},

pages = {282--291},

abstract = {BACKGROUND: Early intervention services (EIS) for psychosis have expanded internationally. Yet, the quality of the guidelines to support and monitor them has never been evaluated. We therefore aimed to systematically appraise the quality of EIS guidelines.nnSTUDY DESIGN: We conducted a systematic review of grey literature websites, supplemented by guidelines identified in a prior scoping review. Eligible documents were guidelines focused on/with a section on early intervention or first episode psychosis. Two independent reviewers appraised each guideline using the Appraisal of Guidelines for Research and Evaluation (AGREE II).nnSTUDY RESULTS: Thirty-two guidelines were included. Guidelines varied widely on scores for the AGREE II domains. Many scored high (≥70%) on Scope and Purpose (24/32; 75%) and Clarity of Presentation (22/32; 69%). Only 22% (7/32) scored well on Rigour of Development, primarily due to the lack of methods for evidence identification and appraisal. The lowest scoring domain was Applicability; only two guidelines scored ≥70%, while more than half provided no information on barriers or facilitators to implementation. Stakeholder involvement, especially from service users, was limited in developing EIS-specific guidelines. Guidelines performing consistently well were from large guideline development groups and used established evidence-grading methods.nnCONCLUSIONS: This first systematic appraisal shows that while many EIS guidelines clearly articulate aims and recommendations, substantial methodological and implementation gaps remain. Nonetheless, EIS guidelines score like others in psychiatry. Still, limited stakeholder engagement and applicability may impede consistent, evidence-based EIS delivery. Future guidelines should explicitly describe evidence-based review processes, integrate service user input, and use AGREE II-like tools to enhance their usability and impact.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42422935,

title = {Validation and normative data for the Multilingual Naming Test (MINT) in French-speaking Quebec adults over 40},

author = {Felix-Etienne Colpron-Larin and Etienne Aumont and Samantha Schwartz and Laura-Maria Perez and Nesrine Rahmouni and Arthur Casa Macedo and Lydia Trudel and Delphine Oliva Lopez and Brandon Hall and Anna Marier and Thomas Carrier and Marie-Anne St-Georges and Jean-Christophe Maranda and Jenna Stevenson and Paolo Vitali and Maxime Montembeault and Pedro Rosa-Neto},

doi = {10.1080/23279095.2026.2700399},

issn = {2327-9109},

year  = {2026},

date = {2026-07-01},

journal = {Appl Neuropsychol Adult},

pages = {1--12},

abstract = {Picture naming tests are critical tools for assessing language and semantic memory deficits in dementia, but must be adapted to local cultural context. This study aimed to develop and validate a Quebec French version of the Multilingual Naming Test (MINT), including determining norms and assessing diagnostic accuracy of mild cognitive impairment (MCI) and dementia. Quebec French-speaking participants ( = 224) were drawn from the TRIAD Montreal cohort and the DEVOCS study and stratified into three subgroups using a double-threshold of quantitative (Montreal Cognitive Assessment) and qualitative (consensus diagnosis) assessments. Linear models were used to create norms and compare diagnostic groups; correspondence with the Boston Naming Test (BNT) used the equipercentile method. Item-specific analysis revealed that naming of three items was sex-dependent. We found significant effects of sex and education, and an interaction trend, on uncued MINT scores. The MINT showed high comparability to the BNT, and Receiver Operating Characteristic curves corroborated their similar diagnostic ability. The MINT performed better at discriminating dementia from cognitively unimpaired participants than at identifying MCI. Correcting for education and sex was necessary to obtain accurate scores. Our results show that the MINT is adequately valid and effective to replace the BNT in neuropsychological assessment in the Quebec French population.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42427711,

title = {Multi-omics characterization of astrocyte subtypes reveals spatially coordinated astrocyte downregulation in depression},

author = {Haruka Mitsuhashi and Harish R Rao and Steffanie Amadei and Anjali Chawla and Maria Antonietta Davoli and Naguib Mechawar and Gustavo Turecki and Corina Nagy},

doi = {10.64898/2026.07.02.735636},

issn = {2692-8205},

year  = {2026},

date = {2026-07-01},

journal = {bioRxiv},

abstract = {Major depressive disorder (MDD) is a complex psychiatric disorder affecting millions of individuals worldwide. Astrocytes, which have been implicated in MDD by several studies, are the most abundant non-neuronal cells in the brain and play critical roles in synaptic regulation, blood-brain barrier maintenance, and immune modulation. While astrocytic molecular and morphological abnormalities are well-established features of MDD, these alterations have not been resolved within their spatial context. Here, we combine spatial transcriptomics with matched snRNA-seq and snATAC-seq datasets to spatially map molecularly distinct astrocyte subtypes and define their regional contributions to MDD pathology. This spatial context further enables the characterization of astrocyte interactions with neighboring cell populations, providing a more holistic assessment of how dysfunctional astrocytes influence local brain microenvironments and circuit function in MDD. We identified spatially localized astrocytic dysfunction in deep cortical layers of the MDD dlPFC, converging across transcriptomic, chromatin, and spatial modalities and centering on the PSAP-GPR37L1 signaling axis. Together, these findings identify astrocyte dysfunction as a key feature of MDD and demonstrate the value of spatially resolved molecular profiling for uncovering how altered astrocyte-neuron communication within deep cortical layers may contribute to disease pathology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42432829,

title = {Group Differences of Multiregion Glutamate Concentration in Clinical High Risk and Schizophrenia},

author = {Shue Kit Man and M Belen Blasco and Razieh Alemi and Samira Raminfard and Pablo M Rusjan and Jamie Near and Deepak K Sarpal and Romina Mizrahi},

doi = {10.1111/ejn.70626},

issn = {1460-9568},

year  = {2026},

date = {2026-07-01},

journal = {Eur J Neurosci},

volume = {64},

number = {1},

pages = {e70626},

abstract = {Glutamatergic changes are one of the characteristic features of psychotic disorders, with changes reported in their clinical high-risk states (CHR), first episode psychosis (FEP), and schizophrenia. Despite the abundance of literature using proton magnetic resonance (H-MRS) to quantify glutamate, the general pattern of changes across different brain regions is not well studied. We investigated the presence of diagnosis group effects on glutamate concentrations in 99 participants in the left dorsal lateral prefrontal cortex, anterior cingulate cortex, associative striatum, and hippocampus using H-MRS in individuals with CHR (n = 31), schizophrenia spectrum psychotic disorder individuals (SCZ) with minimal antipsychotic exposure (n = 30), and healthy controls (n = 38). H-MRS data were normalized against white matter, gray matter, and cerebrospinal fluid fractions within regions of interest (ROI) to quantify local glutamate concentration. Our results showed no significant group differences in glutamate concentration across the four ROIs. Exploratory analyses showed a significant relationship between region and positive symptom severity on glutamate concentration. Post hoc regression analyses revealed that higher positive symptom severity was significantly associated with higher hippocampal glutamate concentrations. We conclude that glutamate concentrations may be related to positive symptoms.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42463550,

title = {Birthweight predicts unfavorable adolescent immunometabolic trajectories leading to adult atypical depression in the ALSPAC cohort},

author = {Qizhou Xia and Carine Parent and Guillaume Elgbeili and Irina Pokhvisneva and Patricia Pelufo Silveira},

doi = {10.1038/s43856-026-01788-z},

issn = {2730-664X},

year  = {2026},

date = {2026-07-01},

journal = {Commun Med (Lond)},

abstract = {BACKGROUND: Lower birthweight, a marker of prenatal adversity, is associated with adverse health outcomes, including psychopathology and immune-metabolic alterations. This study tests whether longitudinal trajectories of chronic immune-metabolic alteration across adolescence, a period of rapid physiological changes, are predicted by birthweight and associated with subsequent depression risk, notably the atypical subtype. We aim to clarify pathways linking prenatal adversity to psychopathology.nnMETHODS: We derived a latent immune-metabolic factor at ages 15, 17, and 24 from standardized C-reactive protein and Homeostatic measurement of insulin resistance in participants from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (N = 3000). We used latent class mixed modeling to identify immune-metabolic trajectory classes. Depression at 24 was measured on the International Classification of Diseases-10 criteria; atypical features were operationalized as the presence of neurovegetative symptoms (e.g. hypersomnia, hyperphagia). Inverse-probability weighting was used to mitigate selection bias.nnRESULTS: Here we show that a four-class quadratic model best fits the data. Membership in the late-adolescence-peaking trajectory is associated with higher odds of depression at 24 (Weighted-Beta=0.767, p = 0.047, OR = 2.15, 95%CI:1.20-3.88), and, notably, of depression with atypical symptoms (Weighted-Beta=1.25, p = 0.0035, OR = 3.50, 95%CI:1.50-8.11). Birthweight is inversely associated with odds of experiencing an unfavourable late-peak trajectory group (Weighted-Beta = -1.99, robust p = 0.0313, OR = 0.14, 95%CI:0.02-0.84). Sex demonstrates a marginal moderating effect (p = 0.050), with the association between birthweight and late-peak trajectory membership being more pronounced in females.nnCONCLUSIONS: Findings provide longitudinal evidence that prenatal adversity, indexed by lower birthweight, predicts individuals experiencing unfavourable adolescent immune-metabolic trajectories that are associated with adult depression, particularly with atypical features. Results suggest that developmental immune-metabolic trajectories could eventually inform patient clinical stratification and point to late adolescence as a possible intervention window.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42471042,

title = {Resting magnetoencephalography alterations in severe mental illnesses: A systematic review},

author = {Fernando Gonzales-Aste and Jessica Ahrens and Dominic Boutet and Hsi Tiana Wei and Sylvain Baillet and Lena Palaniyappan},

doi = {10.1016/j.neubiorev.2026.106867},

issn = {1873-7528},

year  = {2026},

date = {2026-07-01},

journal = {Neurosci Biobehav Rev},

volume = {189},

pages = {106867},

abstract = {Schizophrenia, major depressive disorder (MDD), and bipolar disorder (Severe Mental Illnesses: SMIs), share genetic risk and brain structural changes, but their neural mechanisms remain unclear. Magnetoencephalography (MEG), with millisecond precision, enables direct examination of shared and disorder-specific disturbances in the timing of spontaneous brain activity. We reviewed resting-state MEG evidence on spectral power, connectivity, information-theoretic complexity, and brain dynamics across SMIs. A comprehensive search yielded 62 studies. Three reviewers screened, retrieved, and extracted data on MEG-related variables across regional activity (power), coordination of activity (connectivity, coherence, synchrony), regularity of activity (complexity, entropy), and overall dynamics. Three principal findings come forth. Beta oscillations emerge as a promising, albeit yet unconfirmed, candidate transdiagnostic signal, with increased power now reported across independent investigations of all three disorders and correlating with hallucinations, sleep disturbances, and cognitive deficits, consistent with disrupted predictive processing. However, direct within-study cross-diagnostic comparisons remain sparse (2 of 62 studies). Preliminary support exists for complexity-age dissociation to partition SMIs into neuroprogressive and state-dependent trajectories: neural complexity declines with age in schizophrenia and bipolar disorder (opposite to healthy aging), while depression preserves the normative trajectory. Slow-wave activity diverges sharply: schizophrenia shows a widespread increased slow-wave dominance, while mood disorders show a decrease in activity. We propose a temporal disorganisation spectrum of SMI from excessive fragmentation (schizophrenia) to pathological rigidity (depression), with bipolar disorder occupying an intermediate position. This framework offers biomarker-type utility for stratifying illness severity, tracking neuroprogression, and identifying transdiagnostic therapeutic targets, particularly beta-modulatory neuromodulation interventions applicable across SMIs. Protocol registration: Open Science Framework (http://osf.io/v2gtb/).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42491708,

title = {The Legacy of Seymour Levine},

author = {Michael J Meaney},

doi = {10.1016/j.ynstr.2026.100834},

issn = {2352-2895},

year  = {2026},

date = {2026-07-01},

journal = {Neurobiol Stress},

volume = {43},

pages = {100834},

abstract = {This essay assumes an historical perspective intended to highlight the major contributions of Seymour "Gig" Levine to the conceptual scaffold that guides so much of the current research in development and psychopathology. I suggest that perhaps Levine's most important contribution was to establish an experimental framework that served to transition the clinical observations of Freud and the attachment theories of Bowlby into modern Psychology/Psychiatry.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42521309,

title = {Protecting the brain from post-stroke cognitive impairment and dementia with multimodal exercise training: study protocol for a Bayesian adaptive trial (PROTECT)},

author = {Kevin Moncion and Lynden Rodrigues and Ashanté Bon and Adam Sutoski and Kira Sikorska and Elric Y Allison and Juliano Abreu and Shirin Golchi and Nathalie Arbour and Claudine Gauthier and Caroline Paquette and Pedro Rosa-Neto and Ilana Leppert and Christopher Rowley and Christine L Tardiff and Alexander Thiel and Baraa Al-Khazraji and Ada Tang and Marc Roig},

doi = {10.1136/bmjopen-2026-123336},

issn = {2044-6055},

year  = {2026},

date = {2026-07-01},

journal = {BMJ Open},

volume = {16},

number = {7},

pages = {e123336},

abstract = {INTRODUCTION: Stroke triggers acute vascular and inflammatory mechanisms that predispose the brain to rapid neurodegeneration. Up to 52% of stroke survivors develop cognitive impairment within 6 months and 20% receive a clinical diagnosis of dementia within 5 years. The subacute phase (<6 months) represents a critical window in which the brain may be most responsive to neuroprotective interventions. Multimodal aerobic and resistance training improves cognition in chronic stroke, but whether it improves cognition, neuroimaging markers and blood biomarkers of dementia risk when delivered during this early window remains unknown. The PROTECT trial will compare the effects of 12 weeks of multimodal exercise (moderate-to-high-intensity resistance and aerobic training) versus a low-intensity exercise comparator on cognition, neuroimaging outcomes, blood biomarkers of cognitive decline and dementia risk in people with subacute stroke.nnMETHODS AND ANALYSIS: The PROTECT trial is a 12-week, Phase 3, assessor-blinded, multisite Bayesian adaptive randomised controlled trial (RCT) following a two-arm parallel group sequential design with 6-month and 12-month follow-up (NCT07445841). Participants will be randomised to multimodal training or the comparator using concealed allocation with permuted blocks of varying sizes. The primary outcome is cognition, measured using the 13-item Alzheimer's Disease Assessment Scale-Cognitive assessment (ADAS-Cog-13). Secondary outcomes include ADAS-Cog-Plus, structural and perfusion neuroimaging and blood biomarkers of inflammation and neurodegeneration. Tertiary outcomes include cardiorespiratory fitness, functional mobility, muscle strength, body composition, neuropsychological status, patient-reported cognition, quality of life, fatigue and healthcare utilisation. Outcomes will be assessed at baseline, post-intervention (primary endpoint) and at 6-month and 12-month follow-up. Sample size was estimated via 20 000 Monte Carlo simulations using an ADAS-Cog effect size of Cohen's d=0.63 from a previous exercise RCT. The target was ≥80% power to detect this treatment effect at a one-sided type I error rate of 2.5%, using a weakly informative prior centred at zero with a variance of 100. The minimum required was 45 completers per arm (N=90) and accounting for 25% attrition, up to 120 participants (60 per arm) will be enrolled. Pre-planned adaptive features include: (1) two interim analyses at 50% and 75% of completers; (2) early stopping for efficacy and futility; and (3) sample size re-estimation.nnETHICS AND DISSEMINATION: Ethical approval to conduct this study has been granted by the Centre de recherche interdisciplinaire en réadaptation du Montréal métropolitain (CRIR MP-50-2025-2294) and Hamilton Integrated Research Board (HIREB 19222). Any protocol amendments will be submitted to the appropriate ethics boards. Written informed consent to participate in this study will be obtained from all participants by study coordinators or assistants. Study results will be published and reported in peer-reviewed journal following Adaptive Designs Consolidated Standards of Reporting Trials extension guidelines.nnTRIAL REGISTRATION NUMBER: NCT07445841.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42501784,

title = {Cortical structure and brain size in Thai transfeminine individuals with and without gender-affirming hormone use compared with cisgender heterosexual men, heterosexual women, and gay men},

author = {Malvina N Skorska and Monika Folkierska-Żukowska and Artit Rodkong and Pongpun Saokhieo and Olivier Parent and Daisy Z Hu and Diana E Peragine and Snimar Kaur and Lindsey T Thurston and Taweewat Supintham and Oranicha Kaewthip and Kittichai Wantanajittikul and Gabriel A Devenyi and M Mallar Chakravarty and Suwat Chariyalertsak and Suwit Saekho and Doug P VanderLaan},

doi = {10.1016/j.neuroscience.2026.07.051},

issn = {1873-7544},

year  = {2026},

date = {2026-07-01},

journal = {Neuroscience},

abstract = {Transfeminine individuals' cortical phenotype has been shown to resemble cisgender women's. However, prior studies lacked tests of the generalizability of this finding beyond clinic populations in Europe and the Americas, and of the specificity of this phenotype to gender identity rather than the often-confounding factor of sexual orientation. Also, in clinic-based studies, transfeminine individuals' brain size and cortical thickness have been shown to decrease following the use of gender-affirming hormones (GAH). Focusing on a Thai population, this study provides a test of cross-population generalizability and helps disentangle effects of sex, gender identity, sexual orientation, and self-regulated use of GAH-a widespread but underexamined practice. Brain size and cortical structure were examined in 140 Thai adults (aged 18-44): heterosexual and gay cisgender men, heterosexual cisgender women, and transfeminine individuals attracted to men known locally as sao praphet song ("second kind of woman") with or without histories of GAH use. Regional cortical thickness and, to a limited extent, surface area were associated with gender identity and use of GAH, but not with sexual orientation. Gay men's cortical structure aligned with heterosexual men's. Feminine gender identity-in cisgender women and GAH-naïve sao praphet song-was associated with greater frontal and parietal cortical thickness. Among sao praphet song, GAH use was associated with smaller brain size and thinner cortices. These findings support the generalizability of the previously observed cortical phenotype of transfeminine individuals, and its specificity to gender identity rather than sexual orientation, as well as inform GAH-related brain differences in the context of self-regulated GAH use.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42476460,

title = {Early treatment with naproxen alters hippocampal metabolites in the TgF344-AD rat model of Alzheimer's disease},

author = {Caitlin F Fowler and Elena Osipyan and Gabriel A Devenyi and Dan Madularu and John Breitner and Jamie Near},

doi = {10.1016/j.neuint.2026.106226},

issn = {1872-9754},

year  = {2026},

date = {2026-07-01},

journal = {Neurochem Int},

volume = {199},

pages = {106226},

abstract = {Alzheimer's disease (AD) is characterized by the appearance of brain pathology decades prior to clinical symptoms. The pre-symptomatic phase of AD provides opportunity for early detection and intervention. One early intervention that has been proposed is the use of non-steroidal anti-inflammatory drugs (NSAIDs), such as naproxen. However, evidence suggests that effects of naproxen intervention differ with stage of the disease, and the optimal intervention time is not clear. Accordingly, in this study, we investigated the impact of the timing of naproxen treatment in a rat model of AD. We used the TgF344-AD rat model of AD which develops characteristic pathological features of human AD, including abundant amyloid plaque pathology, astrogliosis, and microgliosis by 6 months of age, and neurofibrillary tangles and neuronal loss by 16 months of age. We examined the effects of naproxen treatment beginning at 1, 4, and 10 months of age in transgenic (Tg) animals and their wild-type (WT) littermates. We used longitudinal in vivo magnetic resonance spectroscopy (MRS) to study the impact of naproxen treatment on hippocampus neurochemistry. Previous studies have used MRS to non-invasively characterize the trajectory of altered hippocampal neurochemistry across the lifespan in the TgF344-AD rat model. In the current study, we employed MRS at 4, 10, and 16 months, i.e. prior to or after the appearance of amyloidosis and gliosis (6 months) and tau pathology (16 months), respectively, in Tg animals. Naproxen treatment altered neurochemistry in Tg animals only if administered beginning at 1 or 4 months of age, mitigating an otherwise observed increase in total choline and decrease in taurine. A more subtle effect was observed on the otherwise-expected increase in myo-inositol. These results highlight the possibility that earlier naproxen intervention could have distinct neurochemical effects compared to delayed treatment, though mechanistic implications remain to be clarified. Moreover, these findings support the use of MRS as a useful non-invasive method of monitoring treatment-related changes in neurochemistry in transgenic animal models.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42499147,

title = {Theoretical and practical challenges for capturing reserve and resilience in aging and Alzheimer's disease: A narrative review},

author = {Valentin Ourry and Maude Wagner and Colin Groot and Rory Boyle and Jacob W Vogel and David Bartrés-Faz and Sylvia Villeneuve},

doi = {10.1002/alz.71664},

issn = {1552-5279},

year  = {2026},

date = {2026-07-01},

journal = {Alzheimers Dement},

volume = {22},

number = {7},

pages = {e71664},

abstract = {The concepts of reserve and resilience in aging and Alzheimer's disease (AD) are widely used but their operationalization remains challenging and often lacks conceptual and methodological consistency. In this narrative review, we describe the chronological history of these concepts and then summarize and discuss key theoretical and practical issues, along with proposed solutions and different perspectives, in the context of aging and AD. Theoretical challenges include risk versus protective factors, dynamic brain and cognitive trajectories, overestimation of resilience and inflection points. Practical challenges include proxy measures, study designs, residual approaches, and influential cases. We highlight the need for greater methodological harmonization, improved validation of proxy, and lifespan longitudinal approaches. Addressing these challenges will strengthen interpretability, reproducibility, and causal inference, ultimately facilitating the translation of reserve and resilience research into preventive and therapeutic strategies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42484771,

title = {Mental health status of sexually diverse youth at age 23: Cross-sectional data from the Quebec Longitudinal Study of Child Development},

author = {Alicia Martineau and Sasha MacNeil and Srividya N Iyer and Kira London-Nadeau and Lauren Anzarouth and Élise Chartrand and Ian Colman and Massimiliano Orri and Nicholas Chadi and Isabelle Ouellet-Morin and Natalie Castellanos Ryan and Annie Pullen Sansfaçon and Robert-Paul Juster and Marie-Claude Geoffroy},

doi = {10.17269/s41997-026-01235-5},

issn = {1920-7476},

year  = {2026},

date = {2026-07-01},

journal = {Can J Public Health},

abstract = {OBJECTIVES: Canadian population-based data show that sexually diverse youth face greater mental health challenges than their heterosexual peers. However, nuances within sexual diversity-particularly among mostly heterosexual persons-are overlooked, and psychotic-like experiences remain underexplored. We examined the mental health of sexually diverse young adults from Quebec, spanning indicators from well-being to psychotic-like experiences.nnMETHODS: Data were drawn from 1324 youth from the Quebec Longitudinal Study of Child Development-a representative cohort born in 1997/98 and followed up until age 23. Participants self-reported their sexual orientation and mental health across nine indicators: suicidality, depression, anxiety, binge drinking, cannabis, other drug use, psychotic-like experiences, well-being, and help-seeking. Standardized mean differences (SMD) assessed group differences, stratified by assigned sex at birth and sexual orientation.nnRESULTS: A total of 324 (24.47%) youth identified as non-heterosexual. These youth reported poorer outcomes across all indicators (SMDs ranged from 0.19 for cannabis use to 0.52 for suicidality) and had higher odds of seeking psychological help (OR = 2.09, 95% CI [1.52-2.89]). Sexually diverse females reported poorer outcomes across all indicators compared to heterosexual females. Sexually diverse males had elevated risks for suicidality, depression, anxiety, and reduced well-being compared to heterosexual males. Mostly heterosexual (N = 156, 48.15%) and bisexual persons (N = 85, 26.23%) reported more symptoms than heterosexuals.nnCONCLUSION: Despite Canada's inclusive stance on sexual diversity, sexually diverse youth-especially those identifying as mostly heterosexual and bisexual-continue to face significant mental health disparities. Our findings highlight the need for accessible, tailored mental health services to support this population.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42476975,

title = {Structural brain complexity is associated with linguistic complexity in psychosis},

author = {Alexandra Korda and Wolfram Hinzen and Rui He and Peter van Dyken and Michael Mackinley and Eric Toyota and Mihai Avram and Christina Andreou and Stefan Borgwardt and Lena Palaniyappan},

doi = {10.1192/j.eurpsy.2026.12242},

issn = {1778-3585},

year  = {2026},

date = {2026-07-01},

journal = {Eur Psychiatry},

pages = {1--30},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid42485844,

title = {Cannabis and tobacco co-use and its association with striatal brain morphometry: Leveraging data from the ENIGMA addiction working group},

author = {Zac J S Yeap and Anthony Juliano and Devarshi Pancholi and Hugh Garavan and Albert Batalla and Janna Cousijn and Francesca Filbey and Edythe D London and Valentina Lorenzetti and Rocio Martin-Santos and Angelica Morales and Nadia Solowij and Murat Yucel and Rachel A Rabin},

doi = {10.1016/j.drugalcdep.2026.113270},

issn = {1879-0046},

year  = {2026},

date = {2026-07-01},

journal = {Drug Alcohol Depend},

volume = {286},

pages = {113270},

abstract = {BACKGROUND: The striatum plays a central role in the pathophysiology of addiction. Studies report that cannabis use is associated with greater striatal gray matter volume (GMV), while tobacco use is associated with both greater and lower striatal GMV. However, their combined effects on striatal GMV remain unclear.nnMETHODS: Using two MRI processing methods, we investigated associations between these substances and striatal GMV. Men and women from eight ENIGMA Addiction sites (N = 302) were parsed into 4 groups; individuals with: co-use (CT, n = 38); cannabis-only use (CO, n = 34); tobacco-only use (TO, n = 61), and controls (CTL, n = 169). Striatal GMV was assessed using (1) Freesurfer-extracted region-specific estimates and (2) voxel-based morphometry using FSL within a striatal mask. Analyses employed 2 × 2 ANCOVAs.nnRESULTS: With Freesurfer, a main effect of cannabis use (CT and CO) emerged in the right nucleus accumbens, and was replicated using FSL (ps ≤ 0.05). With FSL, main effects of cannabis use were found in the putamen and caudate (ps ≤ 0.01), and were modulated by tobacco use (cannabis-tobacco interaction ps ≤ 0.02). Post-hoc comparisons revealed: CT =  CTL >  TO in the putamen and caudate (ps ≤ 0.04); and CTL >  CO (ps ≤ 0.06) and CT >  CO (p = 0.03) in the caudate.nnCONCLUSIONS: Results demonstrate that in the putamen and caudate, individuals who co-use have greater GMV compared to those who use either substance alone, whereas individuals using either substance alone have lower GMV compared to controls. Future research should replicate our novel findings and investigate the clinical correlates of this unique pattern to clarify the functional significance of these findings.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid41865642,

title = {Prevalence and mental health correlates of non-suicidal self-injury in elementary school children},

author = {Shadi Hadj-Youssef and Alessia Civita and Elise Chartrand and Catherine Malboeuf-Hurtubise and Julia Fuoco and Tianna Loose and Isabelle Ouellet-Morin and Nancy Heath and Nathalie Maltais and Imke Baetens and Michel Spodenkiewicz and Sylvana Côté and Marie-Claude Geoffroy},

doi = {10.1016/j.psychres.2026.117097},

issn = {1872-7123},

year  = {2026},

date = {2026-06-01},

journal = {Psychiatry Res},

volume = {360},

pages = {117097},

abstract = {BACKGROUND: Non-suicidal self-injury (NSSI) is relatively common in adolescence and associated with mental health symptoms, yet the prevalence of NSSI and mental health correlates in childhood remain poorly understood.nnOBJECTIVE: Document the lifetime prevalence of NSSI in elementary-school children and concurrent associations with self- and teacher-reported mental health symptoms and peer problems.nnMETHODS: Cross sectional analysis of 859 children (mean age=10.9 years; n = 419 males) from 33 elementary schools in Quebec, Canada who completed a self-report measure of NSSI (5-item Self-Mutilation subscale; Self Harm Inventory) and self- and teacher-report measures of concurrent mental health, including depressive symptoms (Children's Depression Inventory-Short-Form; self-reported only), emotional distress, withdrawal, impulsive/hyperactive/inattentive behaviors, disruptive behaviors, prosocial behaviors, and peer relationship difficulties (victimization) (Social Behavior Questionnaire). Mental health symptoms were transformed into z-scores.nnRESULTS: Lifetime prevalence of NSSI (any method, at least once) was 28.2 %, with no sex differences between males (26.7 %) and females (29.4 %) (p=.403), with scratching being the most frequently reported method (17.2 %). Children reporting NSSI had significantly poorer mental health across indicators examined in both self- and teacher reports, although associations were generally smaller for teacher-reported symptoms. To illustrate, for 1 standard deviation increase in self-reported symptom scores, odds of NSSI were 2.31 times higher for depressive symptoms (95 % CI 1.82-2.92), and 1.70 times higher for peer victimization (95 % CI 1.46-1.99). Associations were stronger among children endorsing multiple NSSI methods compared to those reporting only one.nnCONCLUSION: NSSI (especially scratching) is present in late childhood and associated with worse mental health symptoms and peer problems.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}