Impaired fasting glucose is associated with increased regional cerebral amyloid.
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.
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Jill K
JK
Morris
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Eric D
ED
Vidoni
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Heather M
HM
Wilkins
Department of Molecular and Integrative Physiology, University of Kansas School of Medicine, Kansas City, KS, USA.
Ashley E
AE
Archer
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Nicole C
NC
Burns
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Rainer T
RT
Karcher
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Rasinio S
RS
Graves
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Russell H
RH
Swerdlow
Department of Molecular and Integrative Physiology, University of Kansas School of Medicine, Kansas City, KS, USA.
John P
JP
Thyfault
Department of Neurology and Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA. Electronic address: jburns2@kumc.edu.
Jeffrey M
JM
Burns
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000209:etiology*; D000682:Amyloid / Q000378:metabolism*; D053327:Apolipoprotein E4 / Q000235:genetics; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D005215:Fasting / Q000097:blood*; D005260:Female; D005838:Genotype; D006579:Heterozygote; D006801:Humans; D008297:Male; D012306:Risk; D012307:Risk Factors
D000682:Amyloid; D053327:Apolipoprotein E4; D001786:Blood Glucose
Alzheimer's disease; Amyloid; Apolipoprotein E; Dementia; Impaired fasting glucose; Insulin; Metabolism