Aerobic exercise does not reduce amyloid accumulation in elderly, finds PET imaging
There is an increasing interest in the role of exercise in the prevention and treatment of Alzheimer's disease and related cognitive disorders but aerobic exercise remains among the most promising and cost-effective strategies for delaying or preventing cardiovascular complications, cognitive decline and dementia. However, a recent study suggests, a weekly regimen of this activity does nothing to change the status of beta-amyloid buildup in older adults with elevated levels of the marker for Alzheimer's disease (AD). The research has been published in the journal PLOS ONE on January 14, 2021.
The effect of aerobic exercise on the pathophysiological markers of AD, beta-amyloid and tau, have been less well explored. Animal studies indicate exercise may reduce the amyloid burden and modify AD pathophysiology through direct effects on amyloid precursor protein metabolism and indirect effects on neurotrophic factors, neuroinflammation, and oxidative stress. Studies in humans assessing the effect of physical activity on AD pathophysiology are limited and it remains unclear whether the lifestyle behaviors causally influence cerebral amyloid or vice versa, and whether introducing more physical activity through planned exercise can causally mitigate amyloid pathology. Therefore, researchers of the University of Kansas Alzheimer's Disease Center, America, conducted a study to investigate the role of physical exercise to protect brain health in response with age, including the potential to mitigate Alzheimer's-related pathology. They also assessed the effect of 52 weeks of a supervised aerobic exercise program on amyloid accumulation, cognitive performance, and brain volume in cognitively normal older adults with elevated and sub-threshold levels of cerebral amyloid as measured by amyloid PET imaging.
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