APOE4 and extra calories
Scientists have found that the "Western diet" accelerates the development of Alzheimer's disease
Eating fatty and high-calorie foods significantly accelerates the development of Alzheimer's disease and increases the likelihood of its occurrence in carriers of dangerous mutations in genes associated with this neurodegenerative disease, scientists say in the article Obesity Accelerates Alzheimer-Related Pathology in APOE4 but Not APOE3 Mice, published in the Journal of Neuroscience.
"The APOE4 mutation is the most significant risk factor in the development of Alzheimer's disease, but not all its carriers become victims of this disease. This indicates that some other factors are involved in its development. We found that obesity caused by the Western diet contributes to the development of Alzheimer's disease in APOE4 carriers," write Alexandra Moser and Christian Pike from the University of Southern California in Los Angeles (in a press release Poor diet, plus Alzheimer's gene, may fuel disease – VM).
The APOE gene and protein, associated with the metabolism and circulation of cholesterol and other fats in the body, are one of the most important molecules in the cells of the brain and other organs. Mutations in this gene, as recent studies show, are associated with the development of Alzheimer's disease, atherosclerosis and some other diseases.
For example, the APOE4 mutation, which is present in the genome of about 10-12% of the world's inhabitants, increases the likelihood of developing Alzheimer's disease three times. With such a mutation in two copies of APOE, this probability increases by 12 times, that is, the onset of Alzheimer's disease becomes almost inevitable.
Moser and Pike tried to understand exactly how this typo in the protein makes brain cells more vulnerable to the accumulation of protein "garbage" and to mass death. To answer this question, scientists raised several dozen mice, in which their own APOE gene was replaced by a human version. Half of the rodents became carriers of normal copies of this DNA region, and the rest of the mice – APOE4.
By observing the life of mice in different conditions, biologists hoped to understand what leads to the development of Alzheimer's disease and how it can be prevented. For example, they fed mice normal food and fatty and high-calorie food, similar to the diet that is typical for the developed world, trying to find differences in the work and structure of the rodent brain.
Experiments have shown that the cause of the development of Alzheimer's disease in APOE4 carriers is overweight – in the brains of rodents who ate high-calorie food and suffered from obesity, damaged molecules accumulated much faster than in the nerve cells of their relatives with the normal version of APOE.
On average, the number of beta-amyloid plaques in the hippocampus (memory center) and other parts of the brain of such mice turned out to be about 1.2-1.5 times more when eating a "Western diet" than in all other cases. This, interestingly, was not typical for animals with a normal version of APOE – in these rodents, fatty foods and excess weight did not affect the likelihood of developing Alzheimer's disease in any way.
Biologists do not yet know why this happens, but they suggest that the increased vulnerability of APOE4 carriers to the action of fatty foods may be due to the fact that this gene variant can increase inflammation associated with the development of obesity and other metabolic problems. Revealing the mechanisms of its action, Moser and Pike conclude, will help to finally understand why APOE4 is one of the main risk factors in the development of Alzheimer's disease.
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14.06.2017