An international research team using new bioinformatics techniques reveals a crucial role for myelin and the Gpr17 receptor in brain aging.
A study coordinated by Arthur Butt of the University of Portsmouth with the Universities of Padua, Dusseldorf and the University of Milan allowed to reconstruct the causes of brain aging, identifying myelin as the primary target of the alterations associated with aging, and placed the bases for future studies of "rejuvenation" of myelin-producing cells.
"Everyone - explains Butt - knows the gray matter well, but less than the white one, despite the fact that it represents the other half of the brain. The white matter is the part underneath the gray matter and is composed of axons, the 'electrical cables' of the brain that they connect the various parts of the brain. The axons are covered with a substance called myelin, an insulator which, similar to the plastic of electrical cables, has the task of isolating the axons and therefore facilitating the transmission of information through them ".
Myelin is produced by specialized brain cells called oligodendrocytes: the lack of myelin has devastating effects on brain activity and neurodegenerative diseases are an example of this.
"We compared the brain genome of young and old mice in order to identify which processes are altered in aging - adds Andrea Rivera, of the University of Padua -. These analysis techniques have shown how the decrease in oligodendrocytes in the elderly brain is linked to a loss of brain stem cells called Precursor Oligodendrocytes, essential for the repopulation of oligodendrocytes and myelin. Furthermore, we have identified the G17 gene as the most altered gene in the elderly brain. The loss of Gpr17 reduces the ability of the Precursor Oligodendrocytes to restore the lost white matter ".
During brain aging, says Maria Pia Abbracchio, of the University of Milan, "a loss of white matter has been observed that precedes the loss of gray matter formed by neurons; the causes of this process are not yet clear".
The study finds that in the elderly the functionality of neurons is altered due to a drastic drop in myelin and the oligodendrocytes that produce it.
"Myelin must be continuously produced throughout the life span - he concludes - but in the elderly brain this process fails: why this occurs is still unknown".
(HANDLE).