Reported chronic high glycemic diet intake predicts amyloid deposition in the precuneus of cognitively normal older adults over one year

Abstract

AbstractBackgroundWe previously reported that high glycemic diet (HGD) was related to cerebral amyloid deposits, a pathologic hallmark of Alzheimer’s disease (AD), in multiple highly metabolic regions of interest (ROI). The purpose of this study was to test high glycemic diet’s relationship with longitudinal change in cerebral amyloid deposition in older adults.MethodsThis longitudinal study included 106 cognitively normal older adults with elevated (n=72) and non‐elevated (n=34) amyloid participating in a one‐year exercise intervention trial. Habitual dietary intake was collected at baseline using the National Cancer Institute’s Diet History Questionnaire (DHQ II) and intake was quantified using Diet*Calc software. We derived a HGD pattern using principal covariates regression (PCovR). Amyloid PET (Florbetapir F18) scans were obtained on a GE Discovery ST‐16PET/CT scanner at baseline and 52‐weeks. MIMNuero software was used to standardize the PET images to the whole cerebellum and calculate tracer standard uptake value ratios (SUVR) in 6 ROIs. One‐year regional SUVR delta scores were calculated. We constructed ordinary least squares regression models to assess HGD’s relationship with continuous regional delta SUVR scores controlling for age, sex, and intervention group assignment. Statistical analyses were performed using R (v. 3.6.2; R Foundation, Vienna, Austria). Statistical significance was set at p < 0.05.ResultsThe participants were 68% female with a mean age of 71.1 ± 5.2 years. In the precuneus, higher intake of the derived HGD pattern (β=0.23, p=0.02), sugar (β=0.24, p=0.01), and total carbohydrate (β=0.22, p=0.03) correlated with more amyloid accumulation. Higher reported intake of carbohydrate as a percentage of total energy was related to more amyloid accumulation in the inferior medial frontal gyrus (β=0.20, p=0.04), posterior cingulate gyrus (β=0.20, p=0.04), precuneus (β=0.21, p=0.04), and superior parietal lobule (β=0.21, p=0.03).ConclusionThe results of this study corroborate our previous findings and suggest a physiological role for HGD in amyloid pathology prior to onset of AD‐related symptoms.