Researchers have succeeded in altering the signs of aging in the mouse genome. Thanks to three genes, mice have regained the visual acuity of their youth.
? This process, which affects all cells, first causes dysfunction before it causes cell death. A level , aging would be felt. The scientific community considers that this is due to the accumulation of epigenetic changes that alter the normal functioning of VIA. .
Scientists at Harvard University School of Medicine come up with an attractive but still controversial idea: to change the time stamps stored in the genome to. Study them , December 2, 2020, does not officially prove this theory, but offers a series of experiments to support it.
Thanks to a cocktail of three genes, they managed to limitand promote their recovery. Mouse with then recovered him .
Three anti-aging genes
Three selected genes, October 4, Sox2 and Klf4 (also noted by OSK) have been used by scientists for about ten years in cell dedifferentiation experiments. This involves transforming a differentiated adult cell into a, a condition that can be described as a minor. Pluripotent stem cells are able to differentiate into several different cell types.
But the principle chosen by Harvard University scientists is not to regenerate cells by playing their identity or differentiation, but to modify their epigenetic markers, more precisely, their methyl groups.
The first experiment concerns the effect of a “gene reprogramming” trio on neuronal regeneration. For this purpose, scientists were interested in retinal ganglion cells, which are part ofoptics behind . With pliers, they damaged the optic nerve in adult mice, then injected OSK genes (three genes in one adenoassociate). This treatment limited the death of damaged neurons, but also stimulated new growth.
In the embryonic form and after birth, neurons are able to regenerate in mice, but this ability disappears over time. Therefore, OSK gene injection had an “aging” effect, restoring neuronal capacity only in young animals.
But that’s not all. Four days after the pliers were injuredaccelerated retinal ganglion cells. The methylation patterns then match the cell patterns at the end of its life. By their actions, OSK genes have simply changed them , but especially around genes associated with and synaptic transmission. Neurons have found a second youth.
Mice that obscure their eyesight
The next experiment is about the diseaseappearing with age: glaucoma. Glaucoma is associated with gradual intraocularly, which damages the optic nerve and leads to progressive vision loss. To mimic the disease in mice, the scientists artificially increased the pressure in the eye by injecting beads into the anterior chamber of the eye. After 21 days, OSK genes were injected. The density of the treated mesh is then more functional than the untreated diseased eye. Mice were also tested for vision, and those treated regained vision, not all, but up to 50% of what they had lost.
In the last experiment, the scientists injected reprogramming genes into the eyes of about-year-old mice. At this age, their vision has already decreased compared to younger people. This is about 15% lower than in mice older than five months. After four weeks of treatment, older mice can be seen as well as younger ones. Himthen the same profile is displayed.
These three experiments show that cells respond to OSK genes by adapting their epigenetic changes to make them more suitable for younger individuals. The success of injections also depends on the presence and activity of demethylases (TET1 and TET2),which removes methyl groups from DNA. For mice with fewer, the results were less impressive.
The desire to rebuild our cells at all costs seems tempting to avoid the damage of time and the diseases it causes. But modulating cells in this way is not without the risk cell regeneration can cause. All the mechanisms involved are not yet understood and experiments need to be repeated before this approach is considered a possible treatment for the effects of aging, especially in the case of degenerative eye diseases.