Lifeboat Foundation

When it comes to regeneration, some animals are capable of amazing feats — if you cut the leg off a salamander, it will grow back. When threatened, some geckos drop their tails as a distraction, and regrow them later.

Other animals take the process even further. Planarian worms, jellyfish, and sea anemones can actually regenerate their entire bodies after being cut in half.

Led by Assistant Professor of Organismic and Evolutionary Biology Mansi Srivastava, a team of researchers is shedding new light on how animals pull off the feat, and uncovered a number of DNA switches that appear to control genes for whole-body regeneration. The study is described in a March 15 paper in Science.

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We recently had the opportunity to interview Dr. Amutha Boominathan from the SENS Research Foundation, at the Ending Age-Related Diseases 2019 conference about her research on mitochondrial repair therapies, the value of animal models, and her views on the future of aging research.

Dr. Amutha Boominathan received both her MSc and her PhD in Biochemistry from the University of Pune and the National Chemical Laboratory in India, respectively. She went on to do postdoctoral work in the U.S. relating to mitochondrial biogenesis at U. Penn and Rutgers University. She has extensively studied mechanisms of fusion and fission in mitochondria, Fe-S cluster biosynthesis, and protein import into mitochondria as part of her postdoctoral fellowship with the American Heart Association.

Currently, Amutha leads the MitoSENS program at SENS Research Foundation in Mountain view, California. Her research group is focusing on understanding mitochondrial DNA (mtDNA) mutations and restoring lost functionality as a result of these mutations by way of the allotopic expression of mitochondrial genes. Inherited mtDNA mutations can result in severe and debilitating diseases, such as NARP, Leigh’s syndrome and MELAS. Even in otherwise healthy individuals, mtDNA mutations accumulate with age. The MitoSENS team has already succeeded in stably expressing the ATP8 gene using their method and is looking forward to tackling each of the 13 mitochondrial protein genes in the coming years. Its goal is to develop safe and effective gene therapies for mitochondrial dysfunction.

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The SENS Research Foundation science team is taking the next step in their work on moving mitochondrial genes into the cell nucleus, a process called allotopic expression. Having proven that they can carry out this task with the ATP8 gene in cells, they are now aiming at proof of principle in mice. This will require the production of transgenic mice, using a novel technology funded by the SENS Research Foundation called the maximally modifiable mouse. This mitochondrial project is being crowdfunded at Lifespan.io: you, I, and everyone else can contribute to advancing the state of the art one step further towards eliminating mitochondrial DNA damage as a cause of aging.

Mitochondria are the power plants of the cell, a herd of organelles descended from ancient symbiotic bacteria. They reproduce by replication and are recycled when damaged by cellular maintenance processes. Mitochondria carry the remnant of the original bacterial DNA, encoding thirteen genes vital to the process by which mitochondria package chemical energy store molecules. Unfortunately mitochondria generate reactive molecules as a byproduct of their operation, and this DNA is less well protected than the DNA of the cell nucleus. Some forms of damage to this DNA can break mitochondrial function in ways that allow the broken mitochondria to outcompete their functional peers, leading to dysfunctional cells that export massive quantities of damaging, oxidative molecules into the surrounding tissue. This contributes to conditions such as atherosclerosis, via the production of significant amounts of oxidized cholesterol in the body.

Allotopic expression of mitochondrial genes will work around this issue by providing a backup source of the proteins necessary to mitochondrial function. It has been demonstrated to work for ND4, and that project has been running for some years at Gensight Biologics to produce a therapy for inherited conditions that involve mutation of that gene. This work must expand, however, to encompass all thirteen genes of interest. So lend a hand, and help the SENS Research Foundation team take the next step forward in this process.

Flushing harmful zombie senescent cells from the body that have become old, fatigued and have ceased to divide has become one of the more prominent proposals in the anti-aging sphere. The hypothesis has generated a stream of animal data to support the theory, and now the Mayo Clinic has results from a human study that suggests they have found drugs that can do the same.

While the main goal of the Phase I trail was not to show the effects of reducing senescent cells in the body the researchers were eager to show that the anti-aging senolytics that were tested in animal studies can work the same way in humans as “so far, there has been no direct demonstration of senescent cell clearance by senolytic drugs in peer-reviewed published human clinical trials,” the authors wrote in EBioMedicine, despite the publication of the first human data in January.

Dasatinib and quercetin were given to 9 patients with diabetes related chronic kidney disease for 3 days in this trial. The drugs cleared participants systems in a matter of a few days, but the effects persisted and the authors reported, “Key markers of senescent cell burden were decreased in adipose tissue and skin biopsied from subjects 11 days after completing the 3-day course of D + Q, as were key circulating SASP factors, compared to before administration of these senolytic drugs.”

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A recent study suggests that circulating glucuronic acid may be a useful predictor of both lifespan and healthspan in humans and mice.

What is glucuronic acid?

Glucuronic acid is a metabolite of glucose and is critical for the detoxification of xenobiotic substances. These are compounds that are not naturally produced, should not normally be in the body, or are present in higher concentrations than normal.