An Israeli study has discovered a biological mechanism that could explain how challenging mental and physical activity can delay the development and onset of Alzheimer’s disease.
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The study led by Dr. Boaz Barak from Tel Aviv Univesity and a team of researchers was published recently in the journal Translational Psychiatry, a unit of Nature magazine.
“Numerous studies on Alzheimer’s patients found a correlation between patients’ lifestyles and the speed at which the disease develops,” said Dr. Barak. “As a rule, the more intellectually stimulating and physically challenging a patient’s lifestyle, the slower the disease develops. What was missing was the biological explanation behind this rule, meaning, what exactly about an environment rich in stimuli actually stalls the disease at the cellular level?”
Alzheimer’s mostly effects individuals over the age of 65 and is usually accompanied by the degeneration of brain cells and memory loss. The incurable disease is characterized by a decrease in the levels of proteins responsible for communication between the nerve cells and the brain.
This decrease in proteins is what harms the patients’ cognitive and physical abilities.
Over the years, it has been proved that the levels of these specific proteins are boosted by exposure to intellectual stimuli and physical activity.
The study was conducted in the lab of Professor Uri Ashery, of the Department of Neurobiology and the Sagol School of Neuroscience at Tel Aviv University, in cooperation with Dr. Noam Shomron and Professor Daniel Michaelson, from Tel Aviv University, and Dr. Eytan Okon from Bar-Ilan University.
The researchers compared the amount of microRNA, the molecules responsible for regulating the amount of proteins in cells, in healthy rodents, to the amount of microRNA in rodents that served as a model for Alzheimer’s disease.
In the process, the team compared the amount of microRNA chains in mice that were raised in stimuli-rich environments to those raised in normal environments.
During the second phase of the study, the scientists compared the number of microRNA chains in mice with Alzheimer’s disease raised in normal conditions and healthy mice of the same age that were also raised in normal conditions. Then during the last phase of their research, the team checked for microRNA chains that had undergone significant changes as a result of the Alzheimer’s, on one hand, and those that had undergone change in the mice exposed to stimulus-rich conditions.
“The same microRNA chains that were found to have changed as a result of Alzheimer’s or stimulating environments are also responsible for the regulation of proteins that affect the communication between nerve cells and the brain,” said Dr. Barak. “The amount of those chains in the cell rose after exposure to Alzheimers and caused a decrease in the amount of proteins, which is liable to damage nerve function in the brain. On the other hand, exposure to stimuli-rich environments showed a decrease in the amount of such microRNA chains, which resulted in an increase in proteins, which could lead to an increase in nerve function in the brain.”
Unknown protein chains
In addition, the team of scientists also discovered a number of microRNA chains that underwent significant changes during the early stages of the disease. This information could be used in the future to establish an early detection test for Alzheimers, one that could be done with a simple blood sample.
“These chains were unknown to scientists previously, and they essential to our understanding of the first stages of the disease at the cellular level. Studies conducted over the last few years have proven that it’s possible to isolate and quantify the amount of various microRNA chains through simple blood tests, and I hope that within the next few years, it will be possible to detect changes to microRNA levels in the brain itself, and not just blood,” said Dr. Barak.
It is feasible, Dr. Barak said, that the findings of the study could be used to create patient-specific treatments, depending on the stage of the individual patient’s disease.
Professor Ashery said: “We already know today that mental and physical exercise improves the condition of Alzheimer’s patients. The same microRNA, that in this case were checked in lab mice that represent a model for Alzheimer’s, not only affect the patients’ condition, but also serve as a kind of control switch in the cells that regulate the proteins responsible for various cellular functions. The findings of the study will allow for further, more concise study of the disease, and enhance our ability to develop appropriate medication.”