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Studying the effects of genetic variations on lifespan across the human genome has allowed researchers to find a way to estimate human lifespan, as well as to advance the scientific understanding of diseases and diseases. cell pathways involved in aging; in which the researchers discovered 21 new genomic regions that influence the lifespan.
International scientists have collaborated to identify genetic life-cycle factors, within the largest genome association to date, combining genetic data from more than 500,000 biobankers and other cohorts with data on the lifetime of the parents of each participant. Rather than studying the effects of one or more genes elected over the lifespan, researchers looked at the entire genome to answer questions in a more open manner and to identify new pathways to explore in the future.
The effects of any given gene are statistically small; it is therefore important to use larger samples to identify life-relevant genes with sufficient weight to have statistical power. Using this sample, the researchers were able to validate 6 previously identified associations between aging and genes such as APOE genes related to the risk of neurodegenerative disease.
The researchers used their results to develop a lifetime polygenic risk score: a unique personalized genomic score to estimate a person's genetic probability of living longer based on the weighted contributions of relevant genetic variants. This polygenic risk score predicted which participants were likely to live longer. According to researchers who only use a person's genetic information, it is possible to identify 10% of people with the most protective genes, who will live on average 5 years longer than the 10% least protected.
Whether genetic variants directly affecting aging processes or affecting the risk of individual diseases that can lead to death, have been studied. Among the common variants, variants found in 1 in 200 people, those associated with Alzheimer's disease, heart disease and smoking were related to overall life span; the associations were not for other cancers suggesting that susceptibility to death caused by other cancers is due to rare genetic variants or the environment. Some variants belong to human history. Such a genetic propensity to smoke was not prejudicial before tobacco use, but natural selection did not take many generations to act on these variants, making these variants still quite common, explains Paul Timmers.
Examination of the types of cells and protein pathways in which genetic variants associate the most pronounced effects of lifespan leads to the discovery of genes that play a key role in fetal brain cells and adult prefrontal cortex cells. specific effects in the pathways related to fat metabolism; emphasize the brain as an important organ in the determination of life span, and offers an opportunity for follow-up studies.
Future studies will examine how identified variants and functional pathways affect lifespan; such as whether these pathways are associated with a single disease with implications for longevity or a broader spectrum of age-related diseases. Additional research may help to better understand their interactions, which could potentially identify methods to slow down aging and the onset of disease and improve the duration and quality of life.
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