Scientists have discovered a molecule capable of protecting memory from age-related changes

As we age, it becomes more difficult for the brain to maintain connections between nerve cells, and inflammatory processes and fat metabolism disorders can accelerate memory deterioration. However, some biological mechanisms seem to help the brain resist these changes. Researchers have discovered a gene associated with the preservation of cognitive functions during aging. About how it can protect the brain and what significance this discovery has for the study of Alzheimer's disease is in the Izvestia article.

A molecule that is linked to the brain's resistance to aging

The scientists were looking for genes whose activity changes in response to synapse loss in the hippocampus of mice. This area of the brain plays an important role in the formation and preservation of memories. In the course of their work, the researchers discovered Pla2g2f, which encodes a secreted enzyme, phospholipase. Prior to this study, the role of the gene in brain function remained unknown. The work was published in the journal Nature Neuroscience.

Researchers have found that Pla2g2f levels increase in the hippocampus as we age, as well as during inflammatory processes in the brain. A similar relationship was found in elderly people who showed signs of pathological changes characteristic of Alzheimer's disease, but at the same time retained cognitive functions. This observation helped scientists to study the possible role of the gene in the brain's resistance to age-related changes.

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How aging affects memory and brain function

One of the signs of age—related cognitive decline is the loss of synapses, connections between nerve cells. These changes are especially important in the hippocampus, which is involved in memory processes. At the same time, inflammation and disorders of lipid metabolism, the processes by which cells process and use fats, can increase in the aging brain.

Microglia, the immune cells of the central nervous system, are one of the participants in these processes. They help maintain healthy brain tissue, remove cellular waste, and keep synapses functioning normally. However, with age, lipid droplets can accumulate inside microglia. According to the authors of the study, this is due to a decrease in the ability of cells to clear tissue of waste, maintain synapses and help neurons.

Such changes can accelerate cognitive decline and increase the risk of conditions associated with memory impairment, including mild cognitive impairment and Alzheimer's disease. Therefore, scientists are studying not only the mechanisms of brain damage, but also biological processes that can counteract these changes.

How did changing Pla2g2f levels affect the brains of mice

To find out what role the gene plays, the researchers used genetic and viral tools to reduce or increase Pla2g2f levels in the brains of aging mice. When the level of the gene was decreased, several signs of brain aging increased at once: loss of synapses, inflammation, lipid metabolism disorders, and accumulation of lipid droplets in neurons and microglia. The maturation of new brain cells also worsened and memory impairments occurred.

The researchers also studied the effect of Pla2g2f on human microglial cells. Increasing the activity of the gene reduced the accumulation of lipid droplets and cholesterol esters, two features that are often observed in microglia in Alzheimer's disease. This result indicates a connection between Pla2g2f and lipid metabolism processes, but by itself does not prove that exposure to the gene will preserve memory in humans.

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Could the discovery help with Alzheimer's disease

Age remains the main risk factor for Alzheimer's disease. The results of the study suggest that Pla2g2f may be involved in mechanisms that help the brain maintain resistance to age-related changes. If scientists can confirm this role and learn how to safely influence the corresponding process, it may become one of the areas of future research on cognitive decline.

The authors consider increasing Pla2g2f activity as a potential strategy for maintaining cognitive function and possibly delaying or preventing mild cognitive impairment and Alzheimer's disease. Researchers are now exploring ways to safely boost the level of the gene in the aging brain and in Alzheimer's disease.

However, the results do not yet mean that a way to treat or prevent dementia has been found. Experiments on mice and studies of human microglial cells are not a substitute for clinical trials. To assess the prospects of this approach, scientists will have to find out whether Pla2g2f can be safely affected in the human body and whether this will lead to the preservation of memory and other cognitive functions.