Exercise and Alzheimer’s Disease

As revealed in the Journal of Biological Chemistry “Paper of the Week,” Ayae Kinoshita, a researcher at the Kyoto University Graduate School of Medicine in Japan, exercise is of great significance in fighting against Alzheimer’s disease. Alzheimer’s disease mostly occurs in individuals who are above 65 years of age and is one of the common causes of dementia. This disease is attributed to a number of factors that include the lack of regular exercise as well as an unhealthy diet that includes excess fats.

The research done by Kinoshita included a comparative analysis of voluntary exercise, diet control, and a combination of exercise and diet control in a mouse model with Alzheimer’s disease. Results indicated that regular exercise was of more benefit in reducing formation of β-amyloid—typical characteristic of Alzheimer’s disease — compared to diet control. In addition, exercise triumphed over diet control in restoration of memory loss induced by a fat-rich diet in the mice models. On the basis of this research, the Kyoto University expert recommends that the first priority should be given to exercise in the prevention of Alzheimer’s disease.

 

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One of the distinguishing characteristics of Alzheimer’s disease (AD) is the destruction of brain cells that lead to diminished brain function. Scientists from the University of California at Santa Barbara have discovered what actually happens to these cells in patients with Alzheimer’s and other types of dementia. The findings of the study have been published in The Journal of Biological Chemistry online version.

According to senior author Stuart Feinstein, Ph.D, co-director of UCSB’s Neuroscience Research Institute, brain cells (also known as neurons) stop working properly. Neurons are essential for an individual to perform cognitive skills. The loss of neuronal capacity signals the onset of dementia.

Feinstein, a Molecular, Cellular and Developmental Biology professor, had spent 30 years studying the ‘tau’ protein utilizing cultured cells and test tube bio-chemistry models. Tau is present in long axons which are responsible for connecting neurons and their specific targets. Tau proteins also stabilize microtubules, a component of the cells’ cytoskeleton which is critical to the function and structure of neuronal cells.

For years, it was known that amyloid beta, a type of peptide, can cause the death of neuronal cells and lead to Alzheimer’s disease. The only problem is that it has never been understood how the mechanism that triggers it works. Recent research has shown that amyloid beta requires tau in order to destroy neurons. What is not clear is how it does the action. Most researchers believe that it triggers the excessive chemical modification of tau proteins. For Feinstein, the important goal was to discover the exact details involved in the process of abnormal phosphorylation. By determining what exactly happens, drug companies would have sufficient clues to make the right decisions and pharmaceutical solutions for the problem.

But there is a glitch. The initial hypothesis regarding the effect of amyloid beta on tau phosphorylation was incorrect. What the team discovered was that taking neuronal cells and adding amyloid beta did not result in massively phosphorylated tau proteins. Instead, it resulted in the fragmentation of the proteins within one to two hours and the death of the cells within 24 hours.

According to Feinstein, tau performs multiple jobs, the most widely understood of which is the regulation of cellular cytoskeleton. Cell skeletons, unlike human skeletons, do not undergo abrupt change in its shape. Cell skeletons constantly move, grow and shorten to allow the cell to perform its many functions. The length of cytoskeleton is essential to neurons due to its length.

After the findings, Feinstein’s argument is that the death of neurons that occur in Alzheimer’s is due to a malfunctioning cytoskeleton and that destroying tau proteins can lead to cell death. Feinstein hypothesized the same action that destroys the cytoskeleton in cells treated with cancer drugs could be the same action that was triggered in the neuronal cells.