We could make people less stinky, more resistant to radiation, even less dependent on food and oxygen. But would the new creature be human?
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Category: genetics – Page 449
Autophagy is how our cells recycle their components. Most of the time it runs quietly in the background. But when cells are stressed (such as during fasting or in the presence of dysfunctional proteins) it is increased in order to protect us. Read on to learn about autophagy, its definition and how it works, autophagy regulation, and how to increase autophagy through things like fasting.
Discover the exact, genetic factors in your body that are affecting autophagy with SelfDecode, the most powerful genetic health analysis tool available.
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Evolutionary theory predicts that reproduction entails costs that detract from somatic maintenance, accelerating biological aging. Despite support from studies in human and non-human animals, mechanisms linking ‘costs of reproduction’ (CoR) to aging are poorly understood. Human pregnancy is characterized by major alterations in metabolic regulation, oxidative stress, and immune cell proliferation. We hypothesized that these adaptations could accelerate blood-derived cellular aging. To test this hypothesis, we examined gravidity in relation to telomere length (TL, n = 821) and DNA-methylation age (DNAmAge, n = 397) in a cohort of young (20–22 year-old) Filipino women. Age-corrected TL and accelerated DNAmAge both predict age-related morbidity and mortality, and provide markers of mitotic and non-mitotic cellular aging, respectively. Consistent with theoretical predictions, TL decreased (p = 0.031) and DNAmAge increased (p = 0.007) with gravidity, a relationship that was not contingent upon resource availability. Neither biomarker was associated with subsequent fertility (both p 0.3), broadly consistent with a causal effect of gravidity on cellular aging. Our findings provide evidence that reproduction in women carries costs in the form of accelerated aging through two independent cellular pathways.
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A new interview on LEAF with biogerontologist Dr. João Pedro de Magalhães.
Today, we have an interview with Dr. João Pedro de Magalhães, the biogerontologist who created and runs senescence.info. In the unlikely event that his name is new to you, we had another interview with him last year, which you can check out here.
How do you think we age; are we programmed to die, do we wear out, or is the truth a mixture of both?
I don’t think we wear out. Humans and complex animals are made of cells and molecules that, by and large, have some turnover; we can replace most of our components, so I don’t think it’s correct to see aging as wearing out, at least not in complex animals like humans. (Please see here.) That said, I do think that some forms of cumulative damage contribute to the aging process, such as DNA damage. I also think that there are programmatic aspects to aging. That is, I think that genetic programs coordinating some aspects of growth and development persist into adulthood and become detrimental as forms of antagonistic pleiotropy. It is probably a combination of molecular damage and the inadvertent actions of genetic programs that causes aging.
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Consumer genetic testing company 23andMe announced on Wednesday that GlaxoSmithKline purchased a $300 million stake in the company, allowing the pharmaceutical giant to use 23andMe’s trove of genetic data to develop new drugs — and raising new privacy concerns for consumers.
23andMe is partnering with big pharma company GlaxoSmithKline. Here’s what that means for consumer rights and genetic privacy.
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A new study shows that mice reprogram their gut tissues to repair injury rolling them from an aged state back to a more fetal-like one.
Getting old is one thing; getting old in a healthy way is another. Many elderly people suffer from all kinds of diseases and disorders, ranging from cardiovascular problems and diabetes to Alzheimer’s and Parkinson’s disease. Wouldn’t it be nice if we could keep the body young as we grow older to prevent disease associated with old age? For instance, would it be possible to slow down or reverse the aging processes in the cells of our body?
This question has gained a lot of interest from scientists, and their research has led to the discovery of the important role that the shortening of telomeres, the protective caps on our DNA, plays in aging. While this has been described in recent posts on the LEAF blog, I would like to address another mechanism that has seen an interesting leap forward, more or less by accident: rejuvenation of tissue.
Rejuvenation is a term that has recently been used in the context of senolytics. These are newly discovered compounds that decrease the number of senescent cells in the body. For the purpose of this article, I define rejuvenation as the resetting of a genetic program within a cell or tissue, from adult back to fetal. Typically, cells develop from stem cells, which are cells that can differentiate into many different cell types. During cell differentiation, certain genetic programs in the stem cell are turned off, while others are turned on to make the formation of a specific cell type possible. During rejuvenation, this process is reversed: differentiated cells are reset to an embryonic state.
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