Abstract TP461: Carotid Intima-Media Thickness and Cognition

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Abstract

Background/Objective: Carotid artery intima media thickness (cIMT) may be a marker of cerebral atherosclerotic disease and therefore related to cognitive status in the elderly. We hypothesized that those with greater cIMT would exhibit worse cognition at baseline and have greater cognitive decline over time.

Methods: A sample of 1166 stroke-free community participants from the Northern Manhattan Study (NOMAS) underwent carotid ultrasound and repeated neuropsychological (NP) testing. cIMT was imaged with a standardized B-mode ultrasound protocol and analyzed by a trained sonographer. We used multivariable linear regression to examine cIMT as a correlate of domain-specific NP Z-scores cross-sectionally and over time; we investigated possible effect modification by APOE ε4 allele, adjusting for demographics and vascular risk factors.

Results: The mean age of participants was 71±9 years, 60% were women, 15% white, 18% black, 67% Hispanic, and mean cIMT was 0.93 ± 0.09 mm. NP testing was performed among 1166 participants at baseline and among 826 participants with NP follow-up at a mean of 6.2 years apart. Participants with greater cIMT exhibited worse episodic memory at baseline after adjustment for demographics and vascular risk factors (beta=-0.60, P=0.04). APOE ε4 allele presence was a significant effect modifier, and after stratification, APOE ε4 carriers with greater cIMT exhibited worse episodic memory (beta=-1.26, P=0.04), semantic memory (beta=-1.35, P=0.01), and processing speed (beta=-1.22, P=0.02) at baseline. In longitudinal analysis, participants with greater cIMT at baseline did not exhibit cognitive decline after adjustment for demographics and vascular risk factors, but APOE ε4 allele presence was a significant effect modifier. After stratification, APOE ε4 non-carriers with greater cIMT at baseline exhibited greater declines in executive function (beta=-1.03, P=0.05).

Conclusions: cIMT may be associated with worse cognition and greater cognitive decline in multiple domains among those at high risk for Alzheimer disease, and with worsening executive function in APOE ε4 non-carriers. Interventions that target early stages of atherosclerosis may modify the course of cognitive aging and prevent cognitive decline.

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