Aging is an essential process in the cycle of life . In general, ageing affects the cells, and more specifically, their genetic content.

Of course, this process does not evolve randomly; in fact, not only do we age more or less depending on how we eat and the general lifestyle we lead, but there are also genes that regulate our physical and psychological maturation. In fact, recently an important discovery has been made in this regard: a gene related to the way our brain ages has been found, which is interesting for many reasons that we will now see.

DNA and the maturation of our mind

At the ends of the double helix chain that forms our DNA (enclosed in all the cells of our body) are a series of sequences of nucleic acids that are known as telomeres . Each time a cell divides, these ends are shortened, and when it reaches a certain limit, it causes cell death. The loss of cells is part of aging, which leads to a decrease in the body’s activities.

One of the organs most sensitive to the passage of time is undoubtedly the brain . The loss of neurons takes its toll, and there is a long list of problems that cause this, such as lack of motor coordination or dementia.

In research topics, there has always been a special interest in studying the aging of the brain, for example to reveal its relationship with neurodegenerative diseases such as Parkinson’s or Alzheimer’s. Not long ago, one of these investigations located a gene that is related to this process.

A gene that affects the frontal lobe

The scientists from Columbia University (USA), Asa Abeliovich and Herve Rhinn, examined about 1900 samples of healthy brains. From their observations, they concluded that a gene, called TMEM106B , plays a key role in how human brains age.

Certain varieties of this gene appear to cause the frontal lobe to age at a faster rate than in other people. This is important because this region is involved in executive functions, such as decision-making, managing our focus, or planning. The ageing of the frontal lobe causes a decline in these vital functions and increases the risk of the appearance of diseases known as neurodegenerative diseases.

Genes as risk factors

Finding genes to explain the appearance of biological abnormalities is nothing new. One example is the ApoE gene, responsible for the transcription of the Apolipoprotein E, which in one of its variants (specifically ApoE4) is associated with a greater risk of suffering from Alzheimer’s disease .

The novelty of this discovery is to have found a gene that controls the rhythm of life of a region of the brain. As the discoverers themselves claim, ageing is the main risk factor for neurodegenerative diseases and this research may help to predict the appearance of these diseases or even intervene on them through so-called genetic therapies.

How does this brain aging gene work?

For this study, Asa Abeliovich and Herve Rhinn first obtained genetic data from 1904 autopsy samples of brains that had not suffered from any neurodegenerative disease. Once obtained, they compared them with average data from brains of the same age, looking specifically at 100 genes whose expression increases or decreases with age. The result is that one gene causes differential ageing, the one already called TMEM106B.

The concept of differential age is simple; it is nothing more than a difference between the biological age of the organ (in this case the brain), with the chronological age of the organism. The frontal lobe turns out to be older or younger than the person’s age based on his or her day of birth.

According to its discoverers, the gene TMEM106B begins to manifest its effects from the age of 65, and works to decrease the stress that aging causes on the brain. From what we have seen, there are different alleles, i.e. variants of the gene. Some protect against this stress (their normal function), while others do not perform this task, which causes the process of brain aging to accelerate.

Disease-related

In their study, these researchers also found that a variant of the progranulin gene has an effect on aging, but not as prominent as TMEM106B. Although they are two distinct genes and are found on different chromosomes, both act on the same signaling pathway and are associated with the appearance of a neurodegenerative disease known as frontotemporal dementia .

This clinical syndrome is notable for a degeneration of the frontal lobe, which can extend to the temporal lobe. In adults between 45 and 65, it is the second most common form of dementia after early-onset Alzheimer’s, affecting 15 out of every 100,000 people. In people over 65, it is the fourth most common type of dementia.

However, the study has been conducted from the perspective of healthy brains, so more studies are needed to confirm certain points with their relationships to disease. But, as Abeliovich said, aging makes you more vulnerable to neurodegenerative diseases and vice versa, diseases cause accelerated aging.