4.5 Article

Social Networks and Cerebrospinal Fluid Biomarkers of Alzheimer's Disease Pathology in Cognitively Intact Older Adults: The CABLE Study

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

  1. National Natural Science Foundation of China [91849126]
  2. National Key R&D Program of China [2018YFC1314700]
  3. Taishan Scholars Program of Shandong Province [tsqn20161078]
  4. ZJLab
  5. Tianqiao and Chrissy Chen Institute
  6. State Key Laboratory of Neurobiology and Frontiers Center for Brain Science of Ministry of Education, Fudan University
  7. Shanghai Center for Brain Science and Brain-Inspired Technology
  8. Shanghai Municipal Science and Technology Major Project [2018SHZDZX01]

向作者/读者索取更多资源

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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