Lifeboat Foundation

Who has heard of mitochondrial medicine?

“We know that increased rates of mtDNA mutation cause premature aging,” said Bruce Hay, Professor of biology and biological engineering at the California Institute of Technology. “This, coupled with the fact that mutant mtDNA accumulates in key tissues such as neurons and muscle that lose function as we age, suggests that if we could reduce the amount of mutant mtDNA, we could slow or reverse important aspects of aging.”

This brings us to the second major development relevant to mitochondria in disease — that genetic technology is now at a point where the targeted removal of the problem mitochondrial genes can become the basis for clinical intervention. This is the implication of research that Hay and colleagues both at Caltech and the University of California at Los Angeles described in a paper published in the journal Nature Communications.

Continue reading “Battling Parkinson’s disease” »

For the first time, scientists have added microscopic tracking devices into the interior of cells, giving a peek into how development starts.

For the first time, scientists have introduced minuscule tracking devices directly into the interior of mammalian cells, giving an unprecedented peek into the processes that govern the beginning of development. This work on one-cell embryos is set to shift our understanding of the mechanisms that underpin cellular behavior in general, and may ultimately provide insights into what goes wrong in aging and disease. The research, led by Professor Tony Perry from the Department of Biology and Biochemistry at the University of Bath, involved injecting a silicon-based nanodevice together with sperm into the egg cell of a mouse. The result was a healthy, fertilized egg containing a tracking device. The tiny devices are a little like spiders, complete with eight highly flexible ‘legs’.

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Continue reading “Bill Faloon — If Nothing Else Kills Us, Aging Will (Longevity #005)” »

We’re getting closer to technologies that let us exist forever in some way — using data to power our existence in VR, robots, chatbots and holograms. Should we do it?

Circa 2017 :3

For the first time, scientists have found a genetic mutation that appears to offer a measure of protection against some of the biological effects of ageing.

Continue reading “First Ever Anti-Ageing Gene Discovered in a Secluded Amish Family” »

Sirtuins, telomeres, A.I. experiment with vitamin A and personalized medicine, a bit of everything here.

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Continue reading “BRIAN KENNEDY — Reversing Human Aging (#0004)” »

Space is getting crowded. Aging satellites and space debris crowd low-Earth orbit, and launching new satellites adds to the collision risk. The most effective way to solve the space junk problem, according to a new study, is not to capture debris or deorbit old satellites: it’s an international agreement to charge operators “orbital-use fees” for every satellite put into orbit.

Dr. Michael R. Rose is Professor at Department of Ecology and Evolutionary Biology at University Of California, Irvine. His main area of work has been the evolution of aging.
“Our task is to make nature, the blind force of nature, into an instrument of universal resuscitation and to become a union of immortal beings.“
- Nikolai F. Fedorov

We hold faith in the technologies & discoveries of humanity to END AGING and Defeat involuntary Death within our lifetime.

Continue reading “Dr. Michael R. Rose presents ‘Biological Immortality is REAL’” »

DNA damage is common to our cells, but when we’re young our bodies can fix it pretty easily. Unfortunately we lose that ability over time, leading to many of the symptoms of aging that we know all too well. A new study from MIT has found that reactivating a certain enzyme improves repair of DNA damage in neurons, which helps Alzheimer’s patients and others with cognitive decline.

Previous studies by the team have shown that an enzyme called HDAC1 seems to be involved in DNA repair in neurons. For the new study, the researchers examined what happens when HDAC1 doesn’t do its job.

The team engineered mice to be deficient in HDAC1, and monitored their health compared to normal mice. Things looked good during the animals’ youth – there were no differences in DNA damage or behavior between the two groups. But as they aged, the decline became clear.