期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 81, 期 1, 页码 263-272出版社
IOS PRESS
DOI: 10.3233/JAD-201426
关键词
Alzheimer's disease; biomarkers; cerebrospinal fluid; lifestyle; social network
资金
- National Natural Science Foundation of China [91849126]
- National Key R&D Program of China [2018YFC1314700]
- Taishan Scholars Program of Shandong Province [tsqn20161078]
- ZJLab
- Tianqiao and Chrissy Chen Institute
- State Key Laboratory of Neurobiology and Frontiers Center for Brain Science of Ministry of Education, Fudan University
- Shanghai Center for Brain Science and Brain-Inspired Technology
- Shanghai Municipal Science and Technology Major Project [2018SHZDZX01]
The study found that social networks were closely associated with multiple AD pathological indicators, especially in high-risk populations, suggesting that social networks may have an impact on the metabolism of multiple AD pathologies.
Background: Although social networks are deemed as moderators of incident Alzheimer's disease (AD), few data are available on the mechanism relevant to AD pathology. Objective: We aimed to investigate whether social networks affect metabolism of cerebrospinal fluid (CSF) AD biomarkers during early stage and identify modification effects of genetic factor and subjective cognitive decline (SCD). Methods: We studied participants from the Chinese Alzheimer's disease Biomarker and Lifestyle (CABLE) database who received cognition assessments and CSF amyloid-beta (A beta(1-42) and A beta(1-40)) and tau proteins (total-tau [T-tau] and phosphorylated-tau [P-tau]) measurements. The social networks were measured using self-reported questionnaires about social ties. Linear regression models were used. Results: Data were analyzed from 886 cognitively intact individuals aged 61.91 years (SD = 10.51), including 295 preclinical AD participants and 591 healthy controls. Social networks were mostly associated with CSF indicators of AD multi-pathologies (low P-tau/A beta(1-42) and T-tau/A beta(1-42) and high A beta 1-42/A beta(1-40)). Significant differences of genetic and cognitive status were observed for CSF indicators, in which associations of social network scores with CSF P-tau and indicators of multi-pathologies appeared stronger in APOE 4 carriers (versus non-carriers) and participants with SCD (versus controls), respectively. Alternatively, more pronounced associations for CSF T-tau (beta = -0.005, p < 0.001), A beta(1-42)/A beta(1-40) (beta = 0.481, p = 0.001), and T-tau/A beta(1-42) (beta = -0.047, p < 0.001) were noted in preclinical AD stage than controls. Conclusion: These findings consolidated strong links between social networks and AD risks. Social networks as a modifiable lifestyle probably affected metabolisms of multiple AD pathologies, especially among at-risk populations.
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