Table 2.

Main effect of APOE genotype, main effect of elevated blood glucose (EBG), and interaction between APOE genotype and EBG on neuropathology

	APOE ε4 β ± SE or OR [95% CI]	Elevated Blood Glucose (EBG) β ± SE or OR [95% CI]	Interaction between APOE genotype and EBG p value
AD pathology
Medial temporal AT8 NFT density	2.13 ± 0.77**	1.97 ± 0.88*	0.017
Cortical AT8 NFT density	5.73 ± 1.90**	1.13 ± 2.23	0.179
Medial temporal diffuse plaques (>0)	3.56 [0.95–13.38]	0.93 [0.27–3.23]	0.965
Cortical diffuse plaques (>0)	6.86 [1.26–37.50]*	1.25 [0.34–4.60]	0.973
Medial temporal neuritic plaques (>0)	5.77 [1.52–21.89]**	1.04 [0.33–3.29]	0.964
Cortical neuritic plaques (>0)	10.23 [1.75–59.94]**	1.00 [0.28–3.56]	0.972
Braak and Braak Stage	1.24 ± 0.44**	−0.03 ± 0.52	0.064
Vascular pathology
Atherosclerotic Injury Score	−0.17 ± 0.76	−0.08 ± 0.86	0.119
Atherosclerosis of the circle of Willis (>0)	1.14 [0.37–3.54]	2.87 [0.72–11.42]	0.741
Arteriosclerosis (>0)	1.23 [0.29–5.19]	2.48 [0.45–13.50]	0.973
Cerebral amyloid angiopathy
CAA (>0)	16.76 [1.85–152.13]*	0.60 [0.18–2.00]	0.971

^*p<0.05,

^**p≤0.01

β represents difference in adjusted means; SE = standard error; AD = Alzheimer’s disease; NFT = neurofibrillary tangles; OR = odds ratio; CI = confidence interval; APOE = apolipoprotein E; CAA = cerebral amyloid angiopathy

Main effects and interactions were examined in separate models. All models adjusted for age; sex; time between midlife vascular risk factor assessment and death; and obesity, systolic blood pressure, total cholesterol, and smoking status at midlife.