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Regular Exercise May Keep Your Memory Sharp; These Foods May Help Too!

Regular Exercise May Keep Your Memory Sharp; These Foods May Help Too!

Staying physically fit may help keep Alzheimer's disease at bay, say scientists who found that exercising regularly can improve brain health and prevent decline of vital nerve fibres.

Also, these neuronal changes were reflected in the mice's memory and learning abilities, which also improved.

One of the earlier manifestations of Alzheimer's is the abnormal accumulation of beta-amyloid peptide, which can form large amyloid plaques in the brain and disrupt the function of neuronal synapses.

Verubecestat belongs to a class of experimental Alzheimer's drugs called BACE1 inhibitors that target an enzyme involved in the formation of the toxic amyloid protein that turns into plaques in the brains of Alzheimer's patients.

We still may be some years away from an effective Alzheimer's disease treatment, but all is certainly not lost with many dedicated researchers still working hard to find potentially useful drug targets.

The study was carried out by scientists from the Cleveland Clinic Lerner Research Institute in Ohio.




"Evidence suggests that what is bad for your heart is bad for your brain", noted senior study author Rong Zhang, Ph.D., a professor at UT Southwestern and director of the cerebrovascular laboratory in the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas.

So, in the new study, the researchers wanted to reduce BACE1 more gently and gradually, in the hope that this would yield better results with fewer side effects. And while mice that lacked the enzyme altogether were found to suffer severe neurological defects, those who stopped producing it over time remained healthy.

This was not the only sign of Alzheimer's that the enzyme loss helped to reverse: the mice's levels of beta-amyloid peptide also dropped, and microglia - brain cells that, when activated, had previously correlated with amyloid plaque density - were now deactivated. First, the experiment has only been performed in a mouse model, so there is no guarantee that comparable results will be achieved in humans.

The subsequent offspring also started building up plaque in their brains from quite an early age.

It has raised hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans. However, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.

The findings could be a game changer for the pharmaceutical industry, which has had a rough ride with BACE1 inhibitors - although some analysts claim Merck's failure suggests we are barking up the wrong tree.


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