A growing body of research suggests that physical activity not only improves executive function and cerebral blood flow but may also reduce amyloid and tau levels in the brain.
The new findings were presented here at Alzheimer's Association International Conference (AAIC) 2017.
Much of the focus of this year's AAIC meeting was on lifestyle interventions – healthy eating, reduced stress, adequate sleep, and increased physical activity – to help prevent dementia. Some experts believe that of all lifestyle factors, exercise is tops when it comes to preserving cognition.
In recent years, the identification of biomarkers for Alzheimer's disease (AD) has made it possible to compare levels of amyloid-beta (Aβ) and tau ― both hallmarks of AD ― in those who are and those who are not physically active.
One new study presented here, led by Belinda M. Brown, PhD, School of Psychology and Exercise Science, Murdoch University, Perth, Australia, evaluated the relationship between exercise levels and brain amyloid load in carriers of genetic mutations that cause autosomal-dominant AD.
The analysis included data from the Dominantly Inherited Alzheimer Network for 139 presymptomatic mutation carriers. These patients are destined to develop AD and know approximately when they will start having symptoms.
From self-reports of exercise, the researchers categorized patients into those reporting fewer than 150 minutes per week of (low exercise) and those reporting 150 minutes or more per week (high exercise).
The researchers also had information on brain amyloid load, as quantified by Pittsburgh compound B positron-emission tomography (PiB PET). They stratified patients in order to investigate those with high brain amyloid levels (PiB+).
Compared to the high-exercise group, the low-exercise group was older (38.6 years vs 33.7 years) and had more depressive symptoms, as measured by the Geriatric Depression Scale (2.2 vs 1.4).