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Autophagy (which means “eat yourself”) is a mechanism that allows cells to remove their own components, including unwanted substances that may have entered the body. Researchers at the University of California at Riverside have just discovered that autophagy is not optimal in people with Alzheimer’s disease, pointing to this dysfunction as one of the possible causes of the disease.
According to this new study, the decreased ability of cells to clean themselves is the likely cause of the accumulation of toxic proteins (called aggregates) in the brain. However, according to the most widespread theories, these aggregates are the main cause of dementia, appearing at a certain stage in the development of Alzheimer’s disease.
Along with the signs of dementia, doctors make a definitive diagnosis of Alzheimer’s disease if they find a combination of two things in the brain: amyloid plaques and neurofibrillary tangles. As a reminder, plaques are a collection of beta-amyloid proteins, and the tangles are primarily made up of a protein called tau. All of this causes the death of brain cells and progressive brain atrophy.
For this study, researchers at the University of California at Riverside started from the observation that approximately 20% of people have plaques, but no signs of dementia … which would suggest that the presence of plaques would not be the cause of disease and would not. it necessarily means that a person will have significant symptoms of cognitive decline.
The isomerization of the tau protein at the origin of the difference.
To understand the mechanism behind plaques and tangles, Professor Ryan Julian and his colleagues studied the isomerization of the tau protein, that is, the different forms the molecule can take: an isomer is the same molecule. With a different three-dimensional orientation. of the original. Hands, for example, are isomers because they are mirror images and not exact copies.
For this project, the researchers analyzed all the proteins contained in samples of brains affected or not by the disease. Those who had brain clusters but no dementia had normal tau proteins, while a different form of tau was found in those who had developed plaques or tangles, as well as dementia.
The examination revealed a surprising relationship between the state of Alzheimer’s disease and the isomerization of aspartic acid in a tau peptide. Compared to controls, a striking increase in the abundance of isomers was observed in samples related to Alzheimer’s disease.
Autophagy: protective mechanism
You should know that most of the proteins in the body have a half-life of less than 48 hours. However, if the protein stays in place for too long, some amino acids can convert to the reverse isomer. “If you try to put a right-handed glove on your left hand, it doesn’t work very well. It is a similar problem in biology: the molecules do not work as they should after a while, because a left-handed glove can become a right-handed glove, which is not suitable, “said in a statement, Professor Julian said.
In healthy people, autophagy thus removes worn or defective cells. In this study, the scientists found consistent differences with reduced autophagic flux in Alzheimer’s disease-related samples compared to controls. These results suggest, but do not demonstrate conclusively, that lower autophagic flux may be strongly associated with loss of function in Alzheimer’s brains.
Treatments to improve autophagy are already being tested, and some candidates include existing drugs for cardiovascular disease and other conditions. Before that, previous studies have presented physical exercise and fasting as beneficial in inducing autophagy.
These measures, along with drug treatments, could ultimately help prevent the disease. “If a slowdown in autophagy is the underlying cause, measures that increase it should have the opposite beneficial effect,” Julian said.
Journal of Proteome Research
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