Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment.

TitleCortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment.
Publication TypeJournal Article
Year of Publication2016
AuthorsChung JKu, Plitman E, Nakajima S, M Chakravarty M, Caravaggio F, Gerretsen P, Iwata Y, Graff-Guerrero A
Corporate AuthorsAlzheimer’s Disease Neuroimaging Initiative
JournalJ Geriatr Psychiatry Neurol
Volume29
Issue3
Pagination149-59
Date Published2016 May
ISSN0891-9887
KeywordsAged, Alzheimer Disease, Amyloid beta-Peptides, Aniline Compounds, Cerebral Cortex, Cognitive Dysfunction, Depression, Depressive Disorder, Major, Ethylene Glycols, Female, Humans, Male, Middle Aged, Neuroimaging, Positron-Emission Tomography
Abstract

Depressive symptoms are frequently seen in patients with dementia and mild cognitive impairment (MCI). Evidence suggests that there may be a link between current depressive symptoms and Alzheimer disease (AD)-associated pathological changes, such as an increase in cortical amyloid-β (Aβ). However, limited in vivo studies have explored the relationship between current depressive symptoms and cortical Aβ in patients with MCI and AD. Our study, using a large sample of 455 patients with MCI and 153 patients with AD from the Alzheimer's disease Neuroimaging Initiatives, investigated whether current depressive symptoms are related to cortical Aβ deposition. Depressive symptoms were assessed using the Geriatric Depression Scale and Neuropsychiatric Inventory-depression/dysphoria. Cortical Aβ was quantified using positron emission tomography with the Aβ probe(18)F-florbetapir (AV-45).(18)F-florbetapir standardized uptake value ratio (AV-45 SUVR) from the frontal, cingulate, parietal, and temporal regions was estimated. A global AV-45 SUVR, defined as the average of frontal, cingulate, precuneus, and parietal cortex, was also used. We observed that current depressive symptoms were not related to cortical Aβ, after controlling for potential confounds, including history of major depression. We also observed that there was no difference in cortical Aβ between matched participants with high and low depressive symptoms, as well as no difference between matched participants with the presence and absence of depressive symptoms. The association between depression and cortical Aβ deposition does not exist, but the relationship is highly influenced by stressful events in the past, such as previous depressive episodes, and complex interactions of different pathways underlying both depression and dementia.

DOI10.1177/0891988715606230
Alternate JournalJ Geriatr Psychiatry Neurol
PubMed ID26400248
PubMed Central IDPMC4870393
Grant ListR01 MH084886 / MH / NIMH NIH HHS / United States
U01 AG024904 / AG / NIA NIH HHS / United States
UL1 TR001422 / TR / NCATS NIH HHS / United States
/ / Canadian Institutes of Health Research / Canada
TL1 TR000096 / TR / NCATS NIH HHS / United States