期刊
NEUROBIOLOGY OF AGING
卷 109, 期 -, 页码 135-144出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2021.09.017
关键词
Aging; Medial temporal lobe; Phospho-tau; White matter hyperintensities; Longitudinal; Primary age-related tauopathy
资金
- NIH [R01-AG056014, R01-AG040271, P30-AG010124, R01-EB017255, R01-AG0550 05, RF1AG054409]
- Alzheimer's Association [AARF-19-615258]
- Penn Institute on Aging
- Fondation Philippe Chatrier
- BrightFocus Foundation
The study found that CSF p-tau levels partially mediated the effect of age on hippocampal atrophy rates, while no significant associations were observed for WMHs with temporal lobe structural changes. These results suggest a potential role of tau pathology in age-related MTL structural changes.
Hippocampal atrophy is endemic in 'normal aging' but it is unclear what factors drive age-related changes in medial temporal lobe (MTL) structural measures. We investigated cross-sectional (n = 191) and longitudinal (n = 164) MTL atrophy patterns in cognitively normal older adults from ADNI-GO/2 with no to low cerebral beta-amyloid and assessed whether white matter hyperintensities (WMHs) and cerebrospinal fluid (CSF) phospho tau (p-tau) levels can explain age-related changes in the MTL. Age was significantly associated with hippocampal volumes and Brodmann Area (BA) 35 thickness, regions affected early by neurofibrillary tangle pathology, in the cross-sectional analysis and with anterior and/or posterior hippocampus, entorhinal cortex and BA35 in the longitudinal analysis. CSF p-tau was significantly associated with hippocampal volumes and atrophy rates. Mediation analyses showed that CSF p-tau levels partially mediated age effects on hippocampal atrophy rates. No significant associations were observed for WMHs. These findings point toward a role of tau pathology, potentially reflecting Primary Age-Related Tauopathy, in age-related MTL structural changes and suggests a potential role for tautargeted interventions in age-associated neurodegeneration and memory decline. (C) 2021 Published by Elsevier Inc.
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