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Rejuvenate aging neurons in living organisms? And thus repair the harmful effects of aging on the nervous system? It is no longer a transhumanist fantasy. The feat has just been accomplished in the eyes of the mouse: it was published on 2 December 2020 in the magazine Nature. The researchers injected a (harmless) virus into the animal’s eye that carries three mammalian genes. The infected retinal cells (neurons) then produced a cocktail of three molecules. Results: They were reprogrammed into younger stages. Better yet: in a model of glaucoma, researchers pushed the thin nerve extensions (axons) of these “rejuvenated” neurons far enough back into the optic nerves. As a result, the rodents regained their vision.
The process is inspired by a revolutionary discovery: the one that won the Japanese Nobel Prize in medicine for the Japanese Shinya Yamanaka, in 2012. This doctor-researcher has managed to reprogram the adult cells of any organ (skin, liver, muscles) . , brain …) in immature cells, not specialized but capable of differentiating into any type of cell in the body (these are induced pluripotent stem cells). To accomplish this feat, his team used a cocktail of four genes (OCT3 / OCT4, SOX2, KLF4 and c-MYC). As a sign of its success, the four corresponding proteins will be christened “Yamanaka factors”. In 2008, the Japanese predicted that its discovery could pave the way for tissue regeneration.
Injection of a therapeutic virus
The new study published in Nature offers a first commitment. The authors, from Harvard Medical School (Boston, USA), focused on retinal ganglion cells (RGC). These neurons centralize the visual signals received by the photoreceptors of the eye. They reside in the retina but emit axons that project, through the optic nerve, into the visual areas of the brain.
What if the optic nerve is damaged? If the injury occurs at an early stage of development, its axons will be able to survive and regenerate. But not if it occurs at a mature stage. Hence this question: Could we rejuvenate the RMCs? The researchers started from a premise: senescence and dysfunctions in aging cells are linked to alterations in the “epigenetic signs” that cover their DNA. These signs are small chemical molecules (methyl residues) attached to the DNA at specific points: thus they control the expression of genes and define the identity of each type of cell.
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