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Research shows physical activity can help prevent Alzheimer's

Physical activity is associated with a reduced risk of Alzheimer's disease, according to a study published in Alzheimer’s & Dementia.

The identification of biomarkers for Alzheimer's disease (AD) has made it possible for researchers to compare levels of amyloid-beta and tau ― both hallmarks of AD ― in those who are and those who are not physically active.

A team led by Professor Martin Rossor evaluated the relationship between exercise levels and brain amyloid load in carriers of genetic mutations that cause autosomal-dominant AD – patients destined to develop AD.

From self-reports of exercise, the team categorised 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).

When the entire cohort of mutation carriers was examined, there were no differences in amyloid load between patients in the low-exercise group and those in the high-exercise group. However, for the 16 patients with PiB+ in the low-exercise group, the mean level of brain amyloid was higher than in the 55 patients with PiB+ who were in the high-exercise group.

The researchers were able to show that amyloid-beta in those in the high-exercise group accumulated at a slower rate relative to what would be expected.

Professor Rossor said: “This provides further evidence that exercise is good for brain function and potentially has the ability to delay the onset of AD; and enhance overall cognitive health.”

Visit Alzheimer’s & Dementia to read Habitual exercise levels are associated with cerebral amyloid load in presymptomatic autosomal dominant Alzheimer's disease in full.