Variety in non-pathogenic mitochondrial genes can have lifelong repercussions – quickening the aging process
A collaborative research effort has identified that genetic variability within the 37 genes found inside your mitochondrial genome has a significant impact on metabolism, and even ‘optimal’ aging. This variation is non-pathogenic, meaning that it doesn’t specifically produce a disease as a result, unlike many mitochondrial diseases. It did however affect and influence a more complex web of processes by communicating with the nuclear genome; triggering adaptations and impacting on the rate of aging.
“The key to this study was understanding how the combination and interaction of our two genomes, the nuclear and the mitochondrial, triggers a cellular adaptation with repercussions throughout our lives”
The team discovered that particular variants of mitochondrial genes can trigger cellular adaptation present for the rest of the organism’s life; affecting a range of activity like glucose uptake. Using a mouse model, the scientists showed that mitochondrial variability had a significant impact on the animals’ aging process
A potential treatment
The study raises the possibility of selecting healthy mitochondria for fertilization. Mitochondria are always inherited from the mother, and a new techniques producing ‘3 parent babies’ removes and replaces faulty maternal mitochondria from a similar donor. With greater study of exactly which kinds of variations have a negative or positive effect, we may be able to target a therapy accordingly or even correct and replace mitochondrial genes. Efforts at the SENS foundation on moving the mitochondrial genome to the nucleus could also offer a solution.
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