Researchers from the Mount Sinai School of Medicine (New York) have found that the activity of microglia genes, the brain’s immune cells, is regulated by the SPI1 proto-oncogene, which could become a new target for Alzheimer’s treatment. disease. Article published in the journal Nature Genetics.
The study’s authors used fresh brain tissue samples obtained by biopsy or autopsy from 150 donors with or without Alzheimer’s disease. After isolating the microglia, they sequenced the DNA contained within, which revealed the role of the SPI1 gene.
A change in its activity alters the work of many other genes, and this recreates the work of microglia – all genes involved in this mechanism have been described in detail by the authors of the study. Previously, SPI1 was known as a proto-oncogene; This means that a mutation in it can cause cancer.
Microglia are immune cells found in the brain. However, its functions are much broader than protection against infections, where it is rarely needed, as the brain is separated from the rest of the body by a barrier that neither bacteria nor viruses can penetrate. In recent years, much evidence has emerged regarding the key role of microglia in the development of neurodegenerative diseases, including Alzheimer’s disease.
This is the largest study on microglia, which is very difficult to isolate from the human brain, and is an important step towards understanding the genetic and molecular makeup of Alzheimer’s disease.