76% fewer brain plaques: Why aerobic exercise may be better than any Alzheimer’s disease drug

Brain cells regenerate, inflammation could drop as much as 68% when seniors exercise regularly, rat model shows.

BRISTOL, England — As pharmaceutical companies pour billions into developing new Alzheimer’s treatments, researchers at the University of Bristol and Federal University of São Paulo have uncovered evidence that a far simpler intervention – regular aerobic exercise – might offer comprehensive protection against the disease. Their study reveals how physical activity influences multiple biological pathways involved in this devastating condition.

Amid rising Alzheimer’s rates and limited treatment options, prevention has become increasingly crucial. While current medications may temporarily improve symptoms, they don’t stop the disease’s progression. This makes the study’s findings particularly significant, as they suggest that something as accessible as regular exercise could help combat Alzheimer’s at its biological roots.

“Alzheimer’s is a progressive neurodegenerative disorder with no known cure, impacting millions worldwide,” explains Dr. Augusto Coppi, Senior Lecturer in Veterinary Anatomy at the University of Bristol and one of the study’s senior authors, in a statement. “While physical exercise is known to reduce cognitive decline, the cellular mechanisms behind its neuroprotective effects have remained elusive—until now. This research highlights the potential for aerobic exercise to serve as a cornerstone in preventive strategies for Alzheimer’s.”

Scientists have known that Alzheimer’s involves the accumulation of harmful proteins in the brain, specifically, tau tangles and amyloid plaques. However, this new study, published in Brain Research, reveals that exercise doesn’t just target these problematic proteins — it appears to work through multiple pathways, including reducing brain inflammation and improving the health of cells critical for brain function.

Working with aged rats, researchers implemented an 8-week aerobic exercise program to examine how physical activity affects various markers of brain health. The study focused on the hippocampal formation, a brain region crucial for memory and learning that’s particularly vulnerable in Alzheimer’s disease. By comparing exercising rats to their sedentary counterparts, the team made several striking discoveries about how physical activity impacts brain health at the cellular level.

The results were remarkable. Exercise led to a roughly 63% reduction in tau tangles and an impressive 76% decrease in amyloid plaques compared to sedentary rats. The number of healthy neurons increased by approximately two and a half times in exercising rats. Perhaps most significantly, brain inflammation decreased by 55-68%, depending on the specific inflammatory markers measured.

The research revealed particularly intriguing effects on specialized brain cells called oligodendrocytes, which produce the insulating myelin sheaths that help neurons communicate effectively. The number of healthy oligodendrocytes nearly doubled with exercise, while those showing signs of iron overload — a potential trigger for cell death — were reduced by about 58%. This improvement in oligodendrocyte health suggests exercise helps maintain proper brain cell communication during aging.

The study also examined microglia, the brain’s immune cells that help clean up cellular debris and regulate inflammation. Exercise appeared to optimize these cells’ function, reducing the number of activated inflammatory microglia while increasing those in a more protective state. This suggests that physical activity helps create a healthier environment in the brain by managing inflammation levels.

Beyond just counting cells and measuring protein accumulation, the researchers discovered fascinating relationships between different cell types and markers of brain health. These relationships differed between exercising and sedentary animals, suggesting that physical activity fundamentally changes how brain cells interact with each other and helps restore critical balance in the brain’s function as it ages.

Iron metabolism emerged as a particularly interesting factor in the study. While iron is essential for brain function, its accumulation with age can become problematic. Exercise appeared to help regulate iron levels, potentially protecting brain cells from iron-related damage. This finding has prompted researchers to consider investigating drugs targeting iron metabolism as potential therapeutic approaches for Alzheimer’s.

The implications of these findings extend beyond just Alzheimer’s prevention. They suggest that exercise could potentially help slow or modify the disease’s progression even after it has begun. While human studies would be needed to confirm these benefits, the multiple mechanisms through which exercise appears to work provide hope for its therapeutic potential.

The research team is now planning human clinical trials to confirm these protective effects observed in their rodent models. Additionally, their findings suggest that public health initiatives should prioritize exercise programs specifically tailored to aging populations.

With Alzheimer’s cases projected to rise significantly in coming decades, these findings offer a practical pathway for potential intervention. While the research team continues their investigation through human trials and exploration of iron-targeting drugs, their current findings suggest that integrating regular exercise into daily life could serve as a powerful tool in the growing arsenal against Alzheimer’s disease.