Author(s):
Loureiro, Júlia C. ; Stella, Florindo [UNESP] ; Pais, Marcos V. ; Radanovic, Marcia ; Canineu, Paulo R. ; Joaquim, Helena P.G. ; Talib, Leda L. ; Forlenza, Orestes V.
Date: 2020
Persistent ID: http://hdl.handle.net/11449/201126
Origin: Oasisbr
Subject(s): Alzheimer's disease; Cerebrospinal fluid biomarkers; Geriatric depression; Late-life depression; Mild cognitive impairment; Alzheimer's disease; Alzheimer's disease; Cerebrospinal fluid biomarkers; Cerebrospinal fluid biomarkers; Geriatric depression; Geriatric depression; Late-life depression; Late-life depression; Mild cognitive impairment; Mild cognitive impairment
Description
Made available in DSpace on 2020-12-12T02:24:43Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-07-01
Background: Cognitive impairment is a common feature of late-life depression (LLD). Early studies using Alzheimer's disease (AD) biomarkers inferred a biological link between AD pathology and LLD, but recent findings have challenged this association. The aim of this investigation was to determine a panel of AD-related cerebrospinal fluid (CSF) biomarkers in a cross-section of elders with mild cognitive impairment (MCI) with and without LLD. Methods: Subjects comprised 102 older adults: 27 with ‘pure' amnestic MCI (aMCI), 53 with major depression and cognitive impairment – encompassing 22 late-onset (LOD) and 31 early-onset depression (EOD), and 22 euthymic elders without cognitive impairment (controls). Participants underwent lumbar puncture for determination of CSF concentrations of Aβ1-42, T-tau, and P-tau. Cut-off scores for suspected AD were: Aβ1-42 < 416p g/mL, P-tau > 36.1 pg/mL and Aβ/P-tau ratio < 9.53 (O. V. Forlenza et al. 2015). Statistical analyses consisted of analyses of variance (ANOVA), analyses of covariance (ANCOVA), Bonferroni post-hoc tests, and Pearson's chi-squared tests. Results: ANCOVA (age and schooling as covariates) displayed statistically significant results with respect to CSF biomarkers’ profiles regardless of the socio-demographic divergencies previously identified by one-way ANOVA. Mean Aβ1-42 values (pg/mL) were: aMCI, 360.3 (p < 0.001); LOD, 486.6 (p < 0.001); EOD, 494.2 (p < 0.001); controls, 528.3 (p < 0.001); p< 0.05. Mean Aβ1-42/P-tau ratio: aMCI, 7.9 (p < 0.001); LOD 14.2 (p < 0.001); EOD, 15.3 (p < 0.001); controls, 17.1 (p < 0.001); p < 0.05. Post-hoc tests indicated that patients with aMCI showed significant differences in biomarker profile compatible with AD signature. Limitation: The main limitation is the relatively small sample. Conclusion: Our findings suggest that, distinctively from aMCI, cognitive impairment in LLD is not associated with AD's CSF pathological signature.
Laboratorio de Neurociencias LIM27 Departamento e Instituto de Psiquiatria Hospital das Clinicas HCFMUSP Faculdade de Medicina Universidade de Sao Paulo
UNESP Universidade Estadual Paulista Instituto de Biociências
Programa de Gerontologia Pontifícia Universidade Católica de São Paulo
UNESP Universidade Estadual Paulista Instituto de Biociências
