Glucose Dysregulation Interacts With APOE-∊4 to Potentiate Temporoparietal Cortical Thinning. (February 2016)

• Record Type: Journal Article
• Authors: Foley, Jessica M.; Salat, David H.; Stricker, Nikki H.; McGlinchey, Regina E.; Milberg, William P.; Grande, Laura J.; Leritz, Elizabeth C.
• Is Part Of: American journal of Alzheimer's disease & other dementias. Volume 31:Number 1(2016)
• Page Start: 76
• Page End: 86
• Publication Date: 2016-02
• Subjects: APOE-∊4 -- cortical thickness -- aging -- Alzheimer's disease -- neuroimaging -- diabetes; Alzheimer's disease -- Periodicals; Dementia -- Periodicals; Alzheimer's disease -- Patients -- Care -- United States -- Periodicals; 616.83
• DOI: 10.1177/1533317515587084
• Languages: English
• ISSNs: 1533-3175

Abstract

We examined the interactive effects of apolipoprotein ∊ 4 ( APOE-∊ 4), a risk factor for Alzheimer's disease (AD), and diabetes risk on cortical thickness among 107 healthy elderly participants; in particular, participants included 27 APOE-∊ 4+ and 80 APOE-∊ 4− controls using T1-weighted structural magnetic resonance imaging. Regions of interests included select frontal, temporal, and parietal cortical regions. Among APOE-∊ 4, glucose abnormalities independently predicted reduced cortical thickness among temporoparietal regions but failed to predict changes for noncarriers. However, among noncarriers, age independently predicted reduced cortical thickness among temporoparietal and frontal regions. Diabetes risk is particularly important for the integrity of cortical gray matter in APOE-∊ 4 and demonstrates a pattern of thinning that is expected in preclinical AD. However, in the absence of this genetic factor, age confers risk for reduced cortical thickness among regions of expected compromise. This study supports aggressive management of cerebrovascular factors and earlier preclinical detection of AD among individuals presenting with genetic and metabolic risks.