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Gene therapy, in which artificial genes are integrated with an organism to replace mutated or otherwise deficient genes, has been proposed as a future strategy to prevent aging.[76][77] Targeting catalase to the mitochondria resulted in a 20% lifespan increase in transgenic mice, and improved performance in AAV therapeutically infected mice.[78] In 2012, Israeli researchers from Bar-Ilan University exhibited an increase in lifespan of male mice by over-expression of the SIRT6 gene. In these transgenic mice, levels of proteins involved in the 'insulin-like growth factor 1 (IGF-1)' pathway, which has been previously linked to longevity, were affected by SIRT6 expression.[79] Scientists at the Buck Institute combined mutations in two pathways well known for lifespan extension and report a synergistic five-fold extension of longevity in the nematode C. elegans. The mutations inhibited key molecules involved in insulin signaling (IIS) and the nutrient signaling pathway Target of Rapamycin (TOR). Single mutations in TOR (in this case RSKS-1) usually result in a 30 percent lifespan extension, while mutations in IIS (Daf-2) often result in a doubling of lifespan in the worms. Added together they give a synergistic five-fold increase in lifespan (instead of the expected 130%). The two mutations set off a positive feedback loop in specific tissues that amplified lifespan. Basically these worms lived to the human equivalent of 400 to 500 years.[80] A large number of other distinct genetic modifications affecting autophagy, lipid metabolism, reproduction, and other processes have been reported to extend lifespan in model organisms.[81][82] |
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