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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.

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.

Designer babies are on the horizon after an influential group of scientists concluded that it could be ‘morally permissible’ to genetically engineer human embryos.

In a new report which opens the door to a change in the law, the Nuffield Council on Bioethics, said that DNA editing could become an option for parents wanting to ‘influence the genetic characteristics of their child.’

Although it would be largely used to cure devastating genetic illnesses, or predispositions to cancers and dementia, the experts said they were not ruling out cosmetic uses such as making tweaks to increase height or changing eye or hair colour, if it would make a child more successful.

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Australian researchers have made a discovery about telomeres that may have implications for aging, heart disease, cancer, and other age-related diseases.

So, what are telomeres?

Each of the chromosomes that store our genetic information has a telomere at each end. This protective cap consists of a specific DNA sequence that is repeated thousands of times and has two purposes: firstly, it protects the coding regions of the chromosomes and prevents them from being damaged, and secondly, it acts as a clock that controls the number of replications a cell can undergo; this is thought to act as a quality control system to ensure that aged and potentially damaged cells do not remain in circulation.

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I’m excited to share I’ll be speaking/debating at the upcoming #Biohack the Planet 2018 conference in Oakland on Aug 31 & Sept 1. Many interesting biohackers will be there. Tickets are still available and very reasonably priced right now, but they will likely sell out. Hope to see you there! Here’s the speaker list: http://biohacktheplanet.com/2018-speakers/ #transhumanism #biohacker & ticket page: https://www.eventbrite.com/e/biohack-the-planet-2018-ticket


Bryan Johnson is the founder and CEO of Kernel, OS Fund and Braintree.

In 2016, Bryan invested $100M in Kernel to build advanced neural interfaces to treat disease and dysfunction, illuminate the mechanisms of intelligence, and extend cognition. Kernel is on a mission to dramatically increase our quality of life as healthy lifespans extend. He believes that the future of humanity will be defined by the combination of human and artificial intelligence (HI +AI). In 2014, Bryan invested $100M to start OS Fund which invests in entrepreneurs commercializing breakthrough discoveries in genomics, synthetic biology, artificial intelligence, precision automation, and new materials development. Bryan founded Braintree in 2007, later acquiring Venmo, which he sold to Ebay in 2013 for $800M. He is an outdoor-adventure enthusiast, pilot, and author of a children’s book, Code 7.

BIRMINGHAM, Ala. — Wrinkled skin and hair loss are hallmarks of aging. What if they could be reversed?

Keshav Singh, Ph.D., and colleagues have done just that, in a mouse model developed at the University of Alabama at Birmingham. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks. When the mitochondrial function is restored by turning off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age.

“To our knowledge, this observation is unprecedented,” said Singh, a professor of genetics in the UAB School of Medicine.

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