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

Article type: Research Article

Authors: Ma, Ya-Hui^{a; 1} | Wang, Ya-Yu^{b; 1} | Tan, Lan^{a; 1} | Xu, Wei^a | Shen, Xue-Ning^c | Wang, Hui-Fu^a | Hou, Xiao-He^b | Cao, Xi-Peng^d | Bi, Yan-Lin^e | Dong, Qiang^c | Yang, Jiu-Long^{f; *} | Yu, Jin-Tai^{c; *}

Affiliations: [a] Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China | [b] Department of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Dalian, China | [c] Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China | [d] Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao, China | [e] Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China | [f] Qingdao Municipal Hospital, Qingdao University, Qingdao, China

Correspondence: [*] Correspondence to: Prof. Jin-Tai Yu, MD, PhD, Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, 12th Wulumuqi Zhong Road, Shanghai 200040, China. Tel.: +86 21 52888160; Fax: +86 21 62483421; E-mail: yu-jintai@163.com and Prof. Jiu-Long Yang, Qingdao Municipal Hospital, Qingdao University, No.5 Donghai Middle Road, Qingdao, China. E-mail: waj2002@126.com.

Note: [1] These authors contributed equally to this work

Abstract: 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-β (Aβ1–42 and Aβ1–40) 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/Aβ1–42 and T-tau/Aβ1–42 and high Aβ1–42/Aβ1–40). 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 (β= –0.005, p < 0.001), Aβ1–42/Aβ1–40 (β= 0.481, p = 0.001), and T-tau/Aβ1–42 (β= –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.

Keywords: Alzheimer’s disease, biomarkers, cerebrospinal fluid, lifestyle, social network

DOI: 10.3233/JAD-201426

Journal: Journal of Alzheimer's Disease, vol. 81, no. 1, pp. 263-272, 2021