期刊
NEUROIMAGE-CLINICAL
卷 35, 期 -, 页码 -出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.nicl.2022.103096
关键词
Cognitively normal older adults; Magnetic resonance imaging; White matter lesions; Cognitive decline
类别
资金
- Cana-dian Institutes of Health Research [MFE-176608]
- Healthy Brains for Healthy Lives
- Alzheimer Society Research Program (ASRP)
- Douglas Research Centre (DRC)
- Canada Research Chair
- Canadian Institutes of Health Research Foundation Grant, a Canada Fund for Innovation Grant, an Alzheimer?s Association Grant
- Alzheimer?s society of Canada
- Fonds de recherche Sante Quebec fellowship.Dr
- Canadian In-stitutes of Health research
- Canadian National Science and Engi-neering Research Council, Brain Canada
- Weston Foundation
- Charron
The study found that cerebral small vessel disease (CSVD), amyloid, and pTau are related to age-related cognitive decline. Specifically, there was an inverse correlation between white matter lesions (WMLs) and amyloid AB42, but no correlation between WMLs and pTau. Additionally, baseline AB42 was associated with executive function, while baseline pTau did not have any association with cognitive measures.
Background: Research suggests that cerebral small vessel disease (CSVD), amyloid, and pTau contribute to agerelated cognitive decline. It remains unknown how these factors relate to one another and how they jointly contribute to cognitive decline in normal aging. This project examines the association between these factors and their relationship to cognitive decline in cognitively unimpaired older adults without subjective cognitive decline. Methods: A total of 230 subjects with cerebrospinal fluid (CSF) AB42, CSF pTau181, white matter lesions (WMLs) used as a proxy of CSVD, and cognitive scores from the Alzheimer's Disease Neuroimaging Initiative were included. Associations between each factor and cognitive score were investigated using regression models. Furthermore, relationships between the three pathologies were also examined using regression models. Results: At baseline, there was an inverse association between WML load and AB42 (t = -4.20, p <.001). There was no association between WML load and pTau (t = 0.32, p = 0.75), nor with AB42 and pTau (t = 0.51, p =.61). Correcting for age, sex and education, baseline WML load was associated with baseline ADAS-13 scores (t = 2.59, p =.01) and lower follow-up executive functioning (t = -2.84, p =.005). Baseline AB42 was associated with executive function at baseline (t = 3.58, p<.004) but not at follow-up (t = 1.05, p = 0.30), nor with ADAS-13 at baseline (t = -0.24, p = 0.81) or follow-up (t = 0.09, p = 0.93). Finally, baseline pTau was not associated with any cognitive measure at baseline or follow-up. Conclusion: Both baseline AB42 and WML load are associated with some baseline cognition scores, but only baseline WML load is associated with follow-up executive functioning. This finding suggests that WMLs may be one of the earliest clinical manifestations that contributes to future cognitive decline in cognitively healthy older adults. Given that healthy older adults with WMLs exhibit declines in cognitive functioning, they may be less resilient to future pathology increasing their risk for cognitive impairment due to dementia than those without WMLs.
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