Fight Aging! Newsletter, March 18th 2019
This study provides a possible reason why genes carrying health risks have persisted in human populations. The second found evidence for multiple variants in genes related to ageing that exhibited antagonistic pleiotropic effects. They found higher risk allele frequencies with large effect sizes for late-onset diseases (relative to early-onset diseases) and an excess of variants with antagonistic effects expressed through early and late life diseases.
There also exists other recent tangible evidence of antagonistic pleiotropy in specific human genes. The SPATA31 gene has been found under strong positive genomic selection. Long-lived individuals carry fewer SPATA31 copy numbers. On the other hand, its overexpression in fibroblast cells leads to premature senescence, this being the case in people having multiple copies of the gene. During human evolution, more copies of this gene have likely been favored since this protein is important in sensing and repairing UV-induced DNA damage. Unfortunately, the cost is cell senescence and premature aging.
Austad and Hoffmann: Response to genes that improved fitness also cost modern humans: evidence for genes with antagonistic effects on longevity and disease
Byars and Voskarides, responding to our review of empirical support for the antagonistic pleiotropy theory of the evolution of aging, feel that we have 'failed to acknowledge' recent human studies supporting the theory. Indeed, we mentioned no human studies ...
Source: Fight Aging! - Category: Research Authors: Reason Tags: Newsletters Source Type: blogs
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