2023-12-24 15:17:19
A study has found that lowering the level of a type of cholesterol helps prevent brain damage in people with Alzheimer’s disease.
The study was conducted by researchers at the University of Washington School of Medicine, was conducted on mice, and was published in the journal Neuron, and the website “Neuron” wrote regarding it.Eurek Alert” (EurekAlert).
According to the World Health Organization Dementia A syndrome that can be caused by a number of diseases that cause damage over time to nerve cells, usually leading to a deterioration in the ability to think.
Alzheimer’s disease is the most common type of dementia and may contribute to 60-70% of cases. Although age is the strongest known factor that can cause dementia risk, it is not an inevitable consequence of biological aging.
Studies indicate that people can reduce their risk of dementia by engaging in physical activity and maintaining a healthy lifestyle.
Tau protein
Cognitive deterioration in patients with Alzheimer’s disease and related dementia is driven by excessive accumulation of the protein tau. Wherever this protein accumulates, the decomposition and death of brain tissue begins.
The study revealed that the accumulation of tau protein in the brains of laboratory mice increased the accumulation of a type of fat known as “cholesteryl esters.” It also revealed that reducing these fats helps reduce brain damage and behavioral changes.
Lead researcher, physician and professor David M. Holtzman, said that these results are of great importance in the treatment of Alzheimer’s disease.
He added that the compound that the researchers used to reduce cholesteryl esters results in side effects that make it unsuitable for humans.
He adds that the hope is that a drug will be developed that reduces cholesteryl esters within brain cells without major side effects to be tested on patients with neurodegenerative diseases.
The genetic factor most closely linked to the occurrence of Alzheimer’s is the APOE gene, which activates immune cells in the brain. When they are activated at the wrong time or place, they cause brain damage.
The protein “APOE” plays another important role in the body, which is carrying cholesterol and other fats in the blood, and therefore it has a role in atherosclerosis.
To find out the link between APOE, fat, and brain damage, Dr. Holtzman and researcher Dr. Alexandra Litvinchuk studied laboratory mice that possess genes that make them highly susceptible to the accumulation of tau protein in the brain.
Alzheimer’s symptoms begin in this type of mice at approximately 6 months of age, while significant damage to their brains occurs when they are close to 9 and a half months old, which makes them unable to perform the normal tasks that mice perform to sustain life, such as building nests.
It turned out that the mice in this study either retained the mouse APOE gene, or one of the two human genes, APOE3, which is associated with an average risk of developing Alzheimer’s disease, or the APOE4 gene, was replaced with this gene ( APOE4) is associated with 3 to 4 times the risk of developing Alzheimer’s disease.
Glial cells
The results indicated that the APOE4 gene is linked to problems with fat metabolism in the brain. A large amount of fat has accumulated in abnormal patterns in the brains of mice carrying this gene in the same areas of the brain that were damaged, and the level of more than 180 types of fat in these mice.
Also, immune cells in the brain, known as microglia, were filled with cholesteryl esters, while such results did not appear in mice carrying the APOE3 gene.
Dr. Holtzman pointed out that the microglia cells that were filled with fat became excessively inflamed, causing them to begin secreting things that are harmful to the brain.
Getting rid of these fats may represent a way to reduce inflammation in the brain and reduce nerve damage. To test this, mice were given an experimental drug called “GW3965”, which reduces fats in cells.
This drug led to a clear change and improvement in the condition of mice, but the obstacle that prevents this drug from being given to humans is that the experimental drug has harmful effects on the human liver.
Hope is placed on the tireless efforts made by chemists to design a compound similar to this compound, which does not cause harm to humans.
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