Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease

Abstract

Introduction The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease biomarkers, in a cohort of autosomal dominant Alzheimer's disease (ADAD) mutation carriers. Methods In 139 pre-symptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, CSF Aβ42 and tau levels was evaluated using linear regression. Results No differences in brain amyloid load, CSF Aβ42 or tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e. amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise*estimated years from expected symptom onset was a significant predictor of brain amyloid levels. Discussion Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in ADAD mutation carriers.

Moderate‐ to high‐intensity exercise does not modify cortical β‐amyloid in Alzheimer's disease

“…As outlined previously, different lines of evidence demonstrate the positive effect of exercise on cognitive function and risk of dementia [10][11][12][13][14][15][16][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]. However, the biological mechanisms by which this effect may be mediated remain to be clarified.…”

“…These observations indicate that amyloid PET and CSF measures may reflect different aspects of Aβ biology. It may be further speculated that physical activity affects specific aspects of Aβ biology, which is best captured by one or the other biomarker (e.g., fibrillar vs. soluble Aβ), reflected in the apparently discrepant effect of physical activity on PET‐ versus CSF‐assessed Aβ levels [29]. In a previous study using a subsample from the same randomized controlled trial (RCT) as in the present study, 16 weeks of aerobic exercise did not affect the CSF levels of the AD biomarkers, including Aβ [41].…”

“…Results have been divergent, although most studies have shown a lack of association in both intervention [18][19][20][21][22] and observational studies [23][24][25][26][27][28]. There have been discrepancies in results from observational studies examining the association between Ab or tau and physical activity [29][30][31][32][33][34]. In one study, Ab measured using amyloid PET, but not cerebrospinal fluid (CSF) Ab levels, was associated with physical activity levels [29].…”

Role of physical activity in ameliorating neuropsychiatric symptoms in Alzheimer disease: A narrative review

“…Experimental studies with AD demonstrated that physical exercise can decrease significantly amyloid‐β 42 protein in animal brains . Similarly, human studies indicated that low exercisers had higher mean levels of brain amyloid than high exercisers in autosomal dominant AD mutation carriers and that high‐intensity aerobic exercise decreases plasma concentrations of Aβ 42 in patients with MCI …”

“…80,81 Similarly, human studies indicated that low exercisers had higher mean levels of brain amyloid than high exercisers in autosomal dominant AD mutation carriers and that high-intensity aerobic exercise decreases plasma concentrations of Aβ 42 in patients with MCI. 82 Additionaly, although there are few exercise training and brain volumes studies, there is strong evidence that regular physical exercise can increase plasticity, synaptogenesis, neurogenesis, and volume in several brain regions, including hippocampus, medial temporal lobe, and fronto-parietal regions, which are involved in clinical conditions such as depression, anxiety, agitation, aggression, and disinhibition, respectively. 10,[83][84][85] Similar to BDNF, insulin-like growth factor-1 and vascular endothelial growth factor, which are 2 important factors to modulate neuronal plasticity, especially in the hippocampus, are induced by exercise.…”