Cognitive decline is in part linked to a protein that accumulates in the blood with age, according to a study published Monday, July 6 in the scientific journal Nature Medicine.
The molecule identified as an aging factor is Beta-2 microglubulin (B2M), a component related to the control of the immune system. It would block the regeneration of cells in the hippocampus, the area of the brain linked to memory.
Scientists have studied the brains of older mice and younger mice. They first observed that transfusion of blood from young individuals into older mice improved their cognitive functions and even restored their memory. Based on these results, they speculated that an element of the blood, B2M, could be the cause of cognitive decline. To be sure, they performed the reverse operation and injected blood from older individuals into younger mice. The latter then obtained poorer results on learning and memory tests than young non-transfused mice, suggesting that B2M did indeed act negatively on cognitive functioning and the creation of new neurons.
In additional experiments, the researchers found that the level of B2M increased with age in mice, but also in humans. The molecule has in fact been found in large quantities in the blood and in the cerebrospinal fluid of the brain in elderly people prone to memory and learning disorders.
However, the effect of this aging factor could well be reversed. In young mice which received blood from elderly mice, the action of the molecule disappeared after thirty days after the transfusion. The young mice then found cognitive functions normal. Inhibition of the B2M protein, by a drug or by blocking the gene linked to this molecule would make it possible to stop the aging cognitive. The authors are therefore now working on molecular approaches to target this protein in order to block the cerebral aging that it causes. Great therapeutic hope for neurodegenerative diseases and dementias such as Alzheimer’s disease.
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