564-P: Depressive Symptoms Mediate the Relationship between Diabetes and Cognitive Performance in a Community-Based Sample of Older Adults

Abstract

Objective: To evaluate whether diabetes and prediabetes are associated with reduced cognitive performance among older adults and whether depressive symptoms mediate the association. Methods: We used cross-sectional data from the Einstein Aging Study, a systematically recruited community-based cohort study of diverse older adults (N=794; Mean Age (SD) =78.9 (5.3) years; 64.4% Non-Hispanic White, 28.7% Non-Hispanic Black, 5.7% Hispanic) . Participants were categorized as having diabetes if they reported a history of diabetes, were prescribed a diabetes medication, or had a fasting blood sugar of >126 mg/dL. Those not categorized as having diabetes were identified as having prediabetes if their fasting blood sugar level was 100 to125 mg/dL. Depressive symptoms were assessed using the Geriatric Depression Scale. Cognitive tests include Digit Symbol, Trails-B, Free Recall, Category Fluency, Boston Naming, and Block Design. Linear regression and mediation analyses using the product of coefficients were applied with no diabetes as the comparison group. Results: Compared to those without diabetes, diabetes was associated with worse performance on all cognitive tests (ps<0.05) , except Trails-B (p=0.53) , and increased depressive symptoms (p<0.01) . Prediabetes was not associated with worse cognitive performance or depressive symptoms. For diabetes, evidence of mediation via increased depressive symptoms was observed for Free Recall (p=0.044) , Category Fluency (p=0.033) , and Boston Naming (p=0.048) . Conclusions: Diabetes was consistently associated with worse cognitive performance and depressive symptoms among this older cohort, while prediabetes was not. Mediation results suggest that depressive symptoms may be a biobehavioral pathway linking diabetes and cognition, though the temporal sequence is unclear. Nevertheless, addressing both diabetes and depressive symptoms among older adults may protect cognitive function. Disclosure C.J.Hoogendoorn: None. J.Qin: None. C.Wang: None. N.A.Roque: None. J.Laurenceau: None. M.Katz: None. C.A.Derby: None. R.B.Lipton: Advisory Panel; AbbVie Inc., Biohaven, Eli Lilly and Company, Lundbeck, Consultant; AbbVie Inc., Amgen Inc., Biohaven, Eli Lilly and Company, GlaxoSmithKline plc., Grifols, S.A., Lundbeck, Merck & Co., Inc., Satsuma, Teva Pharmaceutical Industries Ltd., Vedanta, Other Relationship; Wiley-Blackwell, Research Support; AbbVie Inc., Amgen Inc., Axsome, Charleston Labs, Eli Lilly and Company, Gammacore, National Institutes of Health, Satsuma, Teva Pharmaceutical Industries Ltd., Veterans Administration, Stock/Shareholder; Biohaven, CtrlM Health. J.S.Gonzalez: Consultant; Virta Health Corp. Funding This study was supported by grant NIA-P01AG003949 from the National Institutes of Health, the Sylvia and Leonard Marx Foundation and the Hollander Fund. This study was also partially supported by the Einstein–Mount Sinai Diabetes Research Center (P30 DK020541) and the New York Regional Center for Diabetes Translation Research (P30 DK111022) . Dr. Hoogendoorn is also supported by the Drs. David and Jane Willner Bloomgarden Family Fellowship Fund. Dr. Gonzalez is supported by grants RDK104845, RDK121298, RDK121896 and R18 DK098742 from the National Institutes of Health.