Plasma biosignature and brain pathology related to persistent cognitive impairment in late-life depression

Cognitive impairment is highly prevalent among individuals with late-life depression (LLD) and tends to persist even after successful treatment. The biological mechanisms underlying cognitive impairment in LLD are complex and likely involve abnormalities in multiple pathways, or 'cascades,'...

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Bibliographic Details
Published in:Molecular psychiatry 2015-05, Vol.20 (5), p.594-601
Main Authors: Diniz, B S, Sibille, E, Ding, Y, Tseng, G, Aizenstein, H J, Lotrich, F, Becker, J T, Lopez, O L, Lotze, M T, Klunk, W E, Reynolds, C F, Butters, M A
Format: Article
Language:English
Subjects:
Adults
Aged
Aged, 80 and over
Aging
Alzheimer's disease
Atrophy
Benzothiazoles - pharmacokinetics
Biomarkers
Biomarkers - blood
Brain
Brain - diagnostic imaging
Brain - pathology
Cell survival
Cerebrovascular disease
Cerebrovascular diseases
Clotting
Cognition Disorders - etiology
Cognitive ability
Dementia
Dementia disorders
Depression - blood
Depression - complications
Depression - pathology
Emission analysis
Female
Homeostasis
Humans
Image Processing, Computer-Assisted
Immunoassay
Impairment
Inflammation
Interleukin 12
Intracellular
Intracellular signalling
Kinases
Learning algorithms
Machine Learning
Magnetic Resonance Imaging
Male
Medicine
Mental depression
Neuroimaging
Neuropsychological Tests
Older people
Positron emission tomography
Proteins
Proteins - metabolism
Proteomics - methods
Psychiatric Status Rating Scales
Psychiatry
Signal transduction
Stem cell factor
Stem cells
Substantia alba
Substantia grisea
Survival
Tomography
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Summary:Cognitive impairment is highly prevalent among individuals with late-life depression (LLD) and tends to persist even after successful treatment. The biological mechanisms underlying cognitive impairment in LLD are complex and likely involve abnormalities in multiple pathways, or 'cascades,' reflected in specific biomarkers. Our aim was to evaluate peripheral (blood-based) evidence for biological pathways associated with cognitive impairment in older adults with LLD. To this end, we used a data-driven comprehensive proteomic analysis (multiplex immunoassay including 242 proteins), along with measures of structural brain abnormalities (gray matter atrophy and white matter hyperintensity volume via magnetic resonance imaging), and brain amyloid-β (Aβ) deposition (PiB-positron emission tomography). We analyzed data from 80 older adults with remitted major depression (36 with mild cognitive impairment (LLD+MCI) and 44 with normal cognitive (LLD+NC)) function. LLD+MCI was associated with differential expression of 24 proteins (P
ISSN:1359-4184
1476-5578
DOI:10.1038/mp.2014.76