Alzheimer’s-Linked Protein Seems to Respond to Exercise
Everyone knows that exercise is good for you, both physically and mentally. Now, a new study suggests that physical activity may not only boost brainpower, it might even prevent Alzheimer’s disease. Researchers from St. Louis, Missouri, studied mice with an experimental form of Alzheimer’s disease and found that those mice doing the most exercise had the greatest reduction in the toxic protein beta-amyloid.
The study, titled “A spectrum of exercise training reduces soluble Aβ in a dose-dependent manner in a mouse model of Alzheimer’s disease,” appeared on Nov. 10 in the journal Neurobiology of Disease.
Alzheimer’s disease (AD) robs people of their memory and, ultimately, their life due to an accumulation of molecules that destroy brain cells, including the proteins beta-amyloid and hyperphosphorylated tau. About 5.3 million people in the U.S. have AD and an estimated 473,000 will develop the disease this year alone. Five FDA-approved drugs exist to treat this degenerative neurological disease, however, these medications only marginally delay symptoms. They can neither cure AD nor stop its progression.
The scientists, led by Kaitlin M. Moore of Department of Biomedical Sciences, Missouri State University, Springfield, studied mice with an experimental form of Alzheimer’s, known as Tg2576 mice. They examined how three months of low- and high-intensity exercise training affected the accumulation of brain beta-amyloid protein. The exercising mice were given access to a treadmill and were compared to mice with no treadmill access.
The more the mice exercised, the more beta-amyloid cleared from their brains, specifically in a region called the hippocampus that is known to process memory and known to degenerate in AD patients. There were five specific proteins showing increased levels in the brains of active mice, suggesting that physical activity increased these proteins and played a role in amyloid clearance.
The scientists noted in their study, “Five proteins involved in Aβ clearance (neprilysin, IDE, MMP9, LRP1 and HSP70) were elevated by exercise training with its intensity playing a role in each case. Our data demonstrate that exercise training reduces extracellular soluble Aβ in the brains of Tg2576 mice in a dose-dependent manner through an up-regulation of Aβ clearance.”
These results provide more support for the beneficial effects of exercise on the brain and in preventing Alzheimer’s disease. Additional studies of exercise in people are necessary to see if these proteins and their beneficial effects can help prevent Alzheimer’s disease or reduce its effects.