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Abstract Increasing evidences supported that subjective cognitive decline (SCD) might be a potential first symptomatic manifestation of Alzheimer’s disease (AD). The rapidly growing number of SCD individuals who seek medical help and advice also makes it urgent to develop more precise strategy for SCD. Therefore, this study aimed to explore the risk factors for SCD. Logistics and linear regression models were performed to investigate 41 factors for SCD in 1165 participants without objective cognitive impairment. Cochran-Armitage trend test was used to confirm the constant trend toward higher prevalence of SCD with an increasing number of risk factors. A high overall prevalence of SCD was found in total participants (42%). Eight factors were eventually identified as risk factors for SCD, including four stable factors associated with both SCD statues and severity (older age, thyroid diseases, minimal anxiety symptoms, and day time dysfunction; odds ratio (OR) ranging from 1.74 to 2.29) as well as four suggestive factors associated with either SCD statues or severity (female sex, anemia, lack of physical exercises, and living alone; OR ranging from 1.30 to 2.29). The prevalence of SCD gradually increased with the number of risk factors clustering increased in individuals (p for trend

Abstract The bridging integrator 1 (BIN1) gene is the second most important susceptibility gene for late-onset Alzheimer’s disease (LOAD) after apolipoprotein E (APOE) gene. To explore whether the BIN1 methylation in peripheral blood changed in the early stage of LOAD, we included 814 participants (484 cognitively normal participants [CN] and 330 participants with subjective cognitive decline [SCD]) from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database. Then we tested associations of methylation of BIN1 promoter in peripheral blood with the susceptibility for preclinical AD or early changes of cerebrospinal fluid (CSF) AD-related biomarkers. Results showed that SCD participants with significant AD biological characteristics had lower methylation levels of BIN1 promoter, even after correcting for covariates. Hypomethylation of BIN1 promoter were associated with decreased CSF Aβ42 (p = 0.0008), as well as increased p-tau/Aβ42 (p = 0.0001) and t-tau/Aβ42 (p