Scientists have discovered a gene mutation that can reduce the risk of developing Alzheimer’s disease
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Dementia is a syndrome of persistent impairment of cognitive functions due to organic damage to the brain. It often occurs in the elderly. Millions of people around the world suffer from Alzheimer’s disease, one of the types of dementia. Scientists have conducted dozens of studies to better understand this phenomenon, although no one has been able to solve it completely. A group of researchers was probably able to identify a gene mutation that reduces the risk of developing the disease, writes Science Alert. The new study was led by neuroscientist Andy Tsai from Stanford University. Together with colleagues, they tested different variations of the phospholipase C gamma 2 (PLCG2) gene in mice. This was done in order to confirm and trace the mechanism of its connection with Alzheimer’s disease, which scientists discovered earlier. Photo: Illustration of amyloid plaques among neurons and neurofibrillary tangles inside neurons KATERYNA KON/SCIENCE PHOTO LIBRARY/Gettyimages.com Currently, this gene is known to be expressed in the brain’s microglia immune cells. The latter make up only 10-15% of the brain and identify invaders and damaged cells in it. It is PLCG2 that is involved in the signaling between microglia and the induction of the inflammatory response. The gene is triggered when microglia collide with amyloid plaques in the brain, which is what Alzheimer’s disease is usually characterized by. “The microglial response affects neurons, which then affects the ability to learn and form new memories,” explains Indiana University biochemist Gary Landreth. During the experiment, Tsai and the team completely disabled the gene in the animals. When they did, the mice were more likely to develop Alzheimer’s disease. Scientists also noticed that microglia with gene mutations react differently to amyloid plaques. One variant, M28L, acted as a knockout, leaving microglia unable to do their job properly. At the same time, another version of the gene, P522R, was able to support the working memory of mice with a weakened Alzheimer’s disease model and increased PLCG2 protein activity. By allowing microglia to shrink plaques more effectively, the mutation helps clear the way for neurotransmitters to reach their targets in the brains of mice with dementia-like symptoms, the researchers suggest. The theory requires additional tests to confirm. But the new study is consistent with recent suggestions that Alzheimer’s is an immune disease and that the amyloid plaques themselves are not the cause of the malfunction. Overall, the results indicate that promoting microglia’s neuroprotective response to amyloid pathology may limit the progression of Alzheimer’s disease, Tsai and team conclude. Previously, we talked about how dementia can be diagnosed and what to do for those close to you. Read also: Using the Internet during the day can reduce the risk of developing dementia in the elderly – research
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