The
Alzheimer's disease risk gene
apolipoprotein E epsilon 4 (
APOE ε4) 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 ε4 and impaired glycemia on cerebral
amyloid, we stratified nondemented subjects (n = 73) into 4 groups: normal
glucose,
APOE ε4 noncarrier (control [CNT]; n = 31), normal
glucose,
APOE ε4 carrier (E4 only; n = 14) impaired glycemia,
APOE ε4 noncarrier (IG only; n = 18), and impaired glycemia,
APOE ε4 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 ε4 genotype are independent risk factors for regional cerebral
amyloid deposition. However,
APOE ε4 and impaired glycemia did not have an additive effect on cerebral
amyloid.