Scientists have revealed the cause of accelerated brain aging in some people

People with faster cognitive decline were found to have more oligodendrocytes in the brain — cells that form the myelin sheath around nerve fibers. At the same time, the protective layer around the nerves becomes abnormally thickened, while the fibers themselves become thinner. These are the findings of a study published in the journal Nature Medicine.

Oligodendrocytes produce myelin — the sheath that enables nerve signals to be rapidly transmitted throughout the brain. However, scientists reached an unexpected conclusion: an excess of these cells is far from always beneficial and may be associated with age-related impairments in thinking and memory.

The study was based on data from participants in a long-term study of residents of the Scottish Lothian region. Their cognitive abilities were assessed in childhood and then retested after the age of 70. Scientists subsequently examined brain samples from some participants, donated after their death. In the tissues of those whose cognitive functions declined faster, significantly more oligodendrocytes were found, along with clear signs of myelin sheath damage.

Additional experiments on mice helped identify a possible mechanism behind this process. In animals in which the NRF2 gene — responsible for protecting cells from damage — was knocked out in oligodendrocytes, the ability to form memories in a water maze test was noticeably impaired. They also exhibited changes in nerve fibers and myelin similar to those found in humans.

The study authors suggest that disruptions in NRF2 function in oligodendrocytes may play a role in accelerated brain aging. At the same time, this mechanism requires further investigation: the human component of the study identified an association but did not prove a causal relationship, and the tissue analysis covered only a small number of people.

Since NRF2 activity can be modulated using certain drugs, the findings may open new avenues in the search for approaches to preserving cognitive function. However, no medication has yet been tested within this study as a treatment against brain aging.