Impaired fasting glucose is associated with increased regional cerebral amyloid

The Alzheimer's disease risk gene apolipoprotein E epsilon 4 (APOE epsilon 4) is associated with increased cerebral amyloid. Although impaired glucose metabolism is linked to Alzheimer's disease risk, the relationship between impaired glycemia and cerebral amyloid is unclear. To investigate the independent effects of APOE epsilon 4 and impaired glycemia on cerebral amyloid, we stratified nondemented subjects (n = 73) into 4 groups: normal glucose, APOE e4 noncarrier (control [CNT]; n = 31), normal glucose, APOE epsilon 4 carrier (E4 only; n = 14) impaired glycemia, APOE e4 noncarrier (IG only; n = 18), and impaired glycemia, APOE epsilon 4 carrier (IG+E4; n = 10). Cerebral amyloid differed both globally (p = 0.023) and regionally; precuneus (p = 0.007), posterior cingulate (PCC; p = 0.020), superior parietal cortex (SPC; p = 0.029), anterior cingulate (p = 0.027), and frontal cortex (p - 0.018). Post hoc analyses revealed that E4 only subjects had increased cerebral amyloid versus CNT globally and regionally in the precuneus, PCC, SPC, anterior cingulate, and frontal cortex. In IG only subjects, increased cerebral amyloid compared with CNT was restricted to precuneus, PCC, and SPC. IG+E4 subjects exhibited higher cerebral amyloid only in the precuneus relative to CNT. These results indicate that impaired glycemia and APOE e4 genotype are independent risk factors for regional cerebral amyloid deposition. However, APOE epsilon 4 and impaired glycemia did not have an additive effect on cerebral amyloid. (C) 2016 Elsevier Inc. All rights reserved.