Abstract
We examined the impact of physical activity (PA) on longitudinal change in hippocampal volume in cognitively intact older adults at varying genetic risk for the sporadic form of Alzheimer's disease (AD). Hippocampal volume was measured from structural magnetic resonance imaging (MRI) scans administered at baseline and at an 18-month follow-up in 97 healthy, cognitively intact older adults. Participants were classified as High or Low PA based on a self-report questionnaire of frequency and intensity of exercise. Risk status was defined by the presence or absence of the apolipoprotein E-epsilon 4 (APOE-ε4) allele. Four subgroups were studied: Low Risk/High PA (n = 24), Low Risk/Low PA (n = 34), High Risk/High PA (n = 22), and High Risk/Low PA (n = 17). Over the 18 month follow-up interval, hippocampal volume decreased by 3% in the High Risk/Low PA group, but remained stable in the three remaining groups. No main effects or interactions between genetic risk and PA were observed in control brain regions, including the caudate, amygdala, thalamus, pre-central gyrus, caudal middle frontal gyrus, cortical white matter (WM), and total gray matter (GM). These findings suggest that PA may help to preserve hippocampal volume in individuals at increased genetic risk for AD. The protective effects of PA on hippocampal atrophy were not observed in individuals at low risk for AD. These data suggest that individuals at genetic risk for AD should be targeted for increased levels of PA as a means of reducing atrophy in a brain region critical for the formation of episodic memories.
Highlights
Possessing an apolipoprotein-E ε4 (APOE-ε4) allele increases the risk for developing the sporadic form of Alzheimer’s disease (AD) (Bird, 2008)
There were no differences in the number of participants in each group based on physical activity (PA) and Risk classification (p > 0.2)
No significant main or interaction effects were observed for %intracranial volume (ICV) for the hippocampus, thalamus, caudate, caudal middle frontal gyrus, and cortical white matter (WM)
Summary
Possessing an apolipoprotein-E ε4 (APOE-ε4) allele increases the risk for developing the sporadic form of Alzheimer’s disease (AD) (Bird, 2008). We have previously shown that APOE-ε4 status in healthy elders, in combination with measures of hippocampal atrophy obtained at study entry, can predict future cognitive decline after as short an interval as 18 months (Woodard et al, 2010). Such a finding is consistent with the commonly held view that the neuropathology of AD begins decades prior to the clinical diagnosis (Jack, 2012). Another study (Rovio et al, 2005) reported reduced odds of receiving an AD diagnosis in physically active male and female APOE-ε4 carriers compared to inactive carriers In both of these epidemiological studies, the positive effects of PA were not apparent in noncarriers. Etnier and colleagues reported that greater cardiorespiratory fitness was associated with better neurocognitive test performance in healthy older women who were APOE-ε4
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