Anti-aging and neurodegeneration
A compound that slows down aging and brain degeneration has been found
Scientists at the IDOR Institute for Research and Education have discovered a molecule that has the potential to slow the progression of neurodegenerative diseases such as Alzheimer's disease. According to the results of a study published in the journal Translational Psychiatry (Pamplona et al., Age-linked suppression of lipoxin A4 associates with cognitive deficits in mice and humans), a decrease in the level of the substance lipoxin A4 (LXA4) is accompanied by inflammatory processes and cognitive impairment, and its exogenous administration prevents the symptoms of memory loss.
Inflammation is part of the body's defense system, which stops working properly with aging and can contribute to a number of chronic diseases and neurodegenerative disorders, including Alzheimer's disease. Inflammatory reactions are normally controlled by various factors, including lipid molecules lipoxins. These compounds play an important role in wound healing and attracting immune cells to the site of infection. It is also known that lipoxins regulate inflammation in the central nervous system, but the mechanism of their action remained unknown.
In the new work, the researchers assessed the level of lipoxin A4 in the brain of mice, in the culture of human nerve cells and cerebrospinal fluid of patients with dementia and other neurodegenerative diseases. It turned out that LXA4 is produced in significant quantities by neurons and microglia cells — resident macrophages of the central nervous system — in both mice and humans.
With age, the amount of LXA4 in the brain of rodents decreased, which led to deterioration of memory and learning ability in experimental animals. A similar deterioration was observed in mutant animals to which the 5-LOX gene involved in the production of lipoxin A4 was removed. On the contrary, the introduction of exogenous LXA4 through injections weakened the production of cytokines by microglial cells and reversed memory loss in mice in which inflammatory reactions were provoked.
Scientists have demonstrated that the levels of LXA4 in the cerebrospinal fluid of elderly people decrease with dementia. The content of LXA4 correlates with memory indicators, low levels of beta-amyloids and high levels of brain neurotrophic factor (BDNF). Beta-amyloids are considered a neurotoxic factor that provokes Alzheimer's disease, and BDNF stimulates the development of neurons and is important for long-term memory. In general, the results confirmed the key contribution of lipoxin A4 to the protection of the brain, which is impaired with aging and, to a greater extent, with dementia.
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