Abstract MP03: Adiponectin Levels in Young Adulthood and the Association With Midlife Cognition: The Bogalusa Heart Study

Abstract

Objective: Adiponectin (ApN), has anti-inflammatory and anti-atherogenic properties. Low levels of ApN are found even after normalization of glucose in patients with diabetes, and are implicated in atherosclerosis, and dementia onset but results vary across the lifespan. We assessed the relation of ApN levels in young adulthood, with midlife atherosclerosis, measured by carotid intima media thickness (cIMT), and with cognitive function among Black and White individuals from the Bogalusa Heart Study (BHS). Methods: A total of 604 participants from the BHS, a community cohort in rural Louisiana, were examined for ApN levels with lowest quartile of ApN levels (<5.4 μg/mL) defined as low-ApN. Structural equation models assessed mediation via the temporal association of low-ApN (age 36±4) with midlife (age 49±5) cIMT, dichotomized above the 50 th percentile (>0.88mm), and a global cognitive score(GCS) standardized for age, race and sex. Adjusted models included education attendance. Results: Individuals with low-ApN were more likely men [ 56.2% (77), p<0.001] and White [54.7% (75), p<0.001]. No differences in education were found. There was a direct association between low-ApN and GCS (P=0.025), low-ApN and cIMT ≥ 50 th (P=0.001), and cIMT ≥ 50 th and GCS (P=0.002). ( Figure1) In mediation analysis, the ratio of Indirect effect/Total effect was 0.108, indicating that ~11% of the effect of low-ApN on GCS was mediated by cIMT. Education was not associated with low-ApN. Conclusion: Low-ApN levels in early adulthood was associated with poor cognition after ~10 years of follow-up, and the association was partially mediated by subclinical atherosclerosis. This suggests that ApN may play a role in neurodegeneration mechanisms and contribute to the development of dementia, underscoring the importance of addressing cardiometabolic influences earlier in the lifespan to prevent/delay cognitive decline.