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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.

The year is 2050 and researchers have developed an advanced method of replacing 99% of your brain’s functions for digital software/hardware. The process is slow to ensure individuals aren’t simply making copies of themselves. But in return, “digital immortality” has been achieved.


In a future of mind-uploaded “immortals,” will we achieve unlimited freedom or will we simply become slaves to a private entity which owns the data that makes up our own digital minds?

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Published in Scientific Reports, this study is the first to provide evidence of new neuron formation—and the presence of stem cells—in the leopard gecko brain.


University of Guelph researchers have discovered the type of stem cell allowing geckos to create new brain cells, providing evidence that the lizards may also be able to regenerate parts of the brain after injury.

This finding could help in replacing human brain cells lost or damaged due to injury, aging or disease.

“The brain is a complex organ and there are so few good treatments for brain injury, so this is a very exciting area of research,” said Prof. Matthew Vickaryous in the Department of Biomedical Sciences at the Ontario Veterinary College (OVC).

Can technology help us achieve near-everlasting life?


Entrepreneurs in Silicon Valley and beyond are attempting to disrupt what has long been seen as one of the only inevitabilities of life: death.

Computer scientists and artificial intelligence specialists are developing programs that allow people to theoretically avoid death, opening the door to near-everlasting life as well as a myriad of ethical and philosophical questions.

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August 17th sees our friends at UC Berkeley hosting an aging research summit which is shaping up to be pretty interesting.


Please join us for a day of speakers, awards, poster sessions, and valuable networking focused on cutting-edge aging research and technologies. Our aim is no less than to reimagine aging and elder care. A percentage of the proceeds from this event will support scholarships for students interested in research on aging & elder care…

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It’s almost the weekend and what better way to celebrate than a nice long interview with one of the Heroes of aging research? Today we bring you a mega-interview with Dr. Aubrey de Grey.


Today we have an interview with Dr. Aubrey de Grey from the SENS Research Foundation. This interview conducted by Yuri Deigin was originally published in Russian language and he has kindly translated it into English so our audience can enjoy it too.

Yuri: Aubrey, thank you very much for agreeing to this interview. Why don’t we dive right in? I am sure everybody asks you this: how and when did you become interested in aging, and when did you decide to make it your life’s mission to defeat it?

Aubrey de Grey: I became interested in aging and decided to work on it in my late 20s, so, in the early 1990s. The reason I became interested was because that was when I discovered that other biologists were almost all not interested in it. They did not think that aging was a particularly important or interesting question. I had always assumed, throughout my whole life, that aging was obviously the world’s most important problem. I thought that people who understood biology would be working on it really hard. Then, I discovered that wasn’t true and that hardly any biologists were working on it. The ones that were weren’t doing it very well, not very productively as far as I could see. I thought I’d better have a go myself, so I switched fields from my previous research area, which was artificial intelligence.

A new way of administering drugs for wet age-related macular degeneration might be close.


Two studies by researchers at the University of Birmingham have shown that delivering drugs against the wet form of age-related macular degeneration (AMD) in the form of eyedrops might soon be possible in humans [1, 2].

What is age-related macular degeneration?

AMD is a pathology of the retina, which is a light-sensitive tissue located in the back of the eye and is similar to the film in a non-digital camera. Two-dimensional images are created on the retina and are subsequently transferred to the brain in the form of electrical neural impulses. Near the center of the retina is the macula, an oval-shaped region responsible for central, high-resolution, color vision. In AMD, the macula is damaged, impairing or preventing this kind of vision. AMD is progressive, but it cannot lead to total blindness, as it doesn’t affect peripheral vision. It comes in two forms, wet and dry, with the latter being overwhelmingly more common and, unfortunately, presently incurable. As the name suggests, the highest risk factor for AMD is age; the disease is usually observed only in patients over 50.

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.