Lifeboat Foundation: Safeguarding Humanity
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Category: genetics

https://www.youtube.com/watch?v=HOTS0HS7aq4

As part of the LEAF Longevity Bookclub and to celebrate the launch of Dr. David Sinclair’s new book, Lifespan: Why We Age and Why We Don’t Have To, we hosted a special webinar on the 18th of September. The new book takes us on a journey through the biology of why we age and spotlights the exciting research being done in the lab today which could potentially change the way we treat the diseases of aging.

Dr. David Sinclair is a professor of genetics at Harvard Medical School. One of the leading innovators of his generation, he has been named by Time as “one of the 100 most influential people in the world” and in the top 50 most influential people in healthcare. He is a board member of the American Federation for Aging Research and has received more than 35 awards for his research and major scientific breakthroughs. Dr. Sinclair and his work have been featured on 60 Minutes, Today, The Wall Street Journal, The New York Times, Fortune, and Newsweek, among others. He lives in Boston and enjoys hiking and kayaking with his wife and three children.

Multiple prominent personalities and channels, including Joe Rogan, David Pakman, and Utah Public Radio, have interviewed him about his book, and we took the opportunity to allow the community to directly contact him. The webinar was an open event that offered up to 100 people a chance to join the video conference with Dr. Sinclair and to participate in the Q&A session following a reading of some of the exciting sections of the new book. We are delighted to announce that the webinar was an outstanding success, with over 90 people joining the call live to take part as well as many more watching via the livestream on our Facebook page. Five lucky attendees also won a copy of the book courtesy of Dr. Sinclair, and we would like to thank him for this kind offer as well as for taking the time to conduct this webinar with us.

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Carnegie Mellon University computer scientists have taken a deep learning method that has revolutionized face recognition and other image-based applications in recent years and redirected its power to explore the relationship between genes.

The trick, they say, is to transform massive amounts of gene expression data into something more image-like. Convolutional neural networks (CNNs), which are adept at analyzing visual imagery, can then infer which are interacting with each other. The CNNs outperform existing methods at this task.

The researchers’ report on how CNNs can help identify disease-related genes and developmental and genetic pathways that might be targets for drugs is being published today in the Proceedings of the National Academy of Science. But Ziv Bar-Joseph, professor of computational biology and , said the applications for the new method, called CNNC, could go far beyond gene interactions.

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Humans have a maximum natural lifespan of only 38 years, according to researchers, who have discovered a way to estimate how long a species lives based on its DNA.

Scientists at Australia’s national science agency have developed a genetic ‘clock’ computer model that they claim can accurately estimate how long different vertebrates are likely to survive — including both living and extinct species.

Using the human genome, the researchers found that the maximum natural lifespan of humans is 38 years, which matches anthropological estimates of lifespan in early modern humans.

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Is a film based on a video game with fleeting mentions of a biotech buzzword compelling sci-fi? No. But I liked Rampage anyway.

The use of CRISPR to edit genes is perhaps the only novel plot point in this latest monster movie. An evil head of a biotech company subverts a scientist’s work to fashion a bioweapon that revs up the growth hormone gene, and more, in three unfortunate animals. Cue Godzilla, King Kong, and the beast in Lake Placid.

But the screenwriters seem to confuse gene editing with an infectious bioweapon, like anthrax. The tagline at IMDb reveals the befuddlement: “When three different animals become infected with a dangerous pathogen, a primatologist and a geneticist team up to stop them from destroying Chicago.” Infectious disease, genetic modification, or both?

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The idea of a cell therapy for Parkinson’s disease starts out simple: Symptoms of the progressive disease are largely driven by the deaths of dopamine-producing neurons found deep within the brain. With lower levels of the neurotransmitter come the characteristic tremors, rigidity and slow movements.

By replacing those lost nerve cells with new dopamine producers, researchers hope to renew the brain’s connection to the body’s muscles and improve a person’s overall motor function.

But in the brain, everything becomes more complicated. On top of the risk of immune system rejection that comes with any kind of living tissue transplant, it’s important to make sure the implanted cells function correctly and do not pick up any dangerous genetic mutations as they grow.

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Using a targeted gene epigenome editing approach in the developing mouse brain, Johns Hopkins Medicine researchers reversed one gene mutation that leads to the genetic disorder WAGR syndrome, which causes intellectual disability and obesity in people. This specific editing was unique in that it changed the epigenome—how the genes are regulated—without changing the actual genetic code of the gene being regulated.

The researchers found that this gene, C11orf46, is an important regulator during . Specifically, it turns on and off the direction-sensing proteins that help guide the long fibers growing out of newly formed neurons responsible for sending electrical messages, helping them form into a bundle, which connects the two hemispheres of the brain. Failure to properly form this bundled structure, known as the , can lead to conditions such as , autism or other brain .

“Although this work is early, these findings suggest that we may be able to develop future epigenome editing therapies that could help reshape the neural connections in the brain, and perhaps prevent developmental disorders of the brain from occurring,” says Atsushi Kamiya, M.D., Ph.D., associate professor of psychiatry and at the Johns Hopkins University School of Medicine.

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A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.

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Last week, the transhumanist activist Zoltan Istvan announced his candidacy for President of the United States in next year’s elections. The writer, humanitarian and outspoken advocate of radical science is no stranger to the issues surrounding Longevity, and has spoken widely on subjects including AI, genetic editing, technology policy, and futurism.

In 2016, Istvan ran as an independent presidential candidate and travelled across the United States, spreading his message from a coffin-shaped bus, known as the “Immortality Bus.” This time he’s on the ballot, running against Donald Trump as a candidate for the Republican party in next year’s primaries. Things are a bit more serious this time.

Among his key policies, Istvan includes transhumanism, universal basic income and the need to beat China in the global innovation race – an issue we addressed in our Jamie Metzl interview. We spoke to him to find out more about his views on the Longevity sector.

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Lancaster University researchers have discovered, for the first time, how a genetic alteration that increases the risk of developing Autism and Tourette’s impacts on the brain.

Their research also suggests that ketamine, or related drugs, may be a useful treatment for both of these disorders.

Autism affects an estimated 2.8 million people in the UK while Tourette’s Syndrome — a condition that causes a person to make involuntary sounds and movements called tics –affects an estimated 300,000 people in the UK. The treatments available for both disorders are limited and new treatments are urgently required. Recent research has also shown that these disorders are genetically linked.

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