Lifeboat Foundation

“The Foundation has created a unique and transparent mechanism for boosting early longevity research worldwide and ensuring mass public participation in decision making,” said Alex Zhavoronkov, Visionary Board member and an expert in AI-powered drug discovery. “This approach finally allows us to speak about getting closer to the idea of mass adoption of longevity ideas and treatments.”

“Age is the greatest risk factor for nearly every major cause of death and disability in developed nations. Therapeutically targeting biological aging is key to fulfilling the promise of 21st century medicine, and the Foundation is poised to play a central role in making this a reality,” said Matt Kaeberlein, CEO of the American Aging Association and Professor at the University of Washington, where he leads several major initiatives.

“In five years, healthy longevity will not only exist as a lab-proven concept, but will become part of everyone’s life,” said Andrea Maier, Visionary Board member and co-director of the Centre for Healthy Longevity at the National University of Singapore.

According to 2020’s McKinsey Global Survey on artificial intelligence (AI), in 2,020 more than 50% of companies have adopted AI in at least one business unit or function, so we witness the emergence of new AI trends. Organizations apply AI tools to generate more value, increase revenue and customer loyalty. AI leading companies invest at least 20% of their earnings before interest and taxes (EBIT) in AI. This figure may increase as COVID-19 is accelerating digitization. Lockdowns resulted in a massive surge of online activity and an intensive AI adoption in business, education, administration, social interaction, etc.

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DNA extracted from ancient Egyptian mummies is offering an intriguing glimpse at what three men might’ve looked like when they hung out in the Fertile Crescent more than 2,000 years ago.

The genetic sleuthing led to highly detailed 3D constructions of a trio from an ancient Nile community known as the Abusir el-Meleq who are estimated to have lived between 2,023 and 2,797 years ago.

The images result from DNA phenotyping, which predicts a person’s physical characteristics based on genetic data. The re-creations mark the first time comprehensive DNA phenotyping has been performed on human DNA this old, according to Virginia-based Parabon NanoLabs, the company behind the images. Parabon typically taps DNA phenotyping to help solve criminal cases.

Describing one scenario, an AI could act as a quiet bioterrorist. Since we have become heavily dependent on computers and computer-dependent systems are by default dispersed and impersonal, the task of eradicating humanity could be divvied up to gazillions of little micro-players, who may or may not know what they are doing. “For example, the AI could pay employees in a DNA-synthesizing company to do small jobs and then combine their work into creating a biological weapon, such as a virus able to kill a lot of people,” says Turchin.

“How are you certain you are not in a multilevel simulation, where your behavior is being monitored by humans who are testing your benevolence levels?”

Turchin addresses this in one of his letters to the young, future humanity-killing AI. “There are several instrumental reasons why exterminating humanity is not in your interest,” the Russian transhumanist writes. “Cooperating with humans will only increase your chances of accomplishing any goal you may have.”

New research exploring theories of aging has found that small mutations accumulating in DNA are unlikely to be fully responsible for this process.

The research, a collaboration between the Wellcome Sanger Institute, University of Birmingham, University of Edinburgh and others, found that human cells and tissues can accumulate many more mutations than are normally present, without the body showing the features associated with aging.

The new study, published today (30 September) in Nature Genetics, compared DNA taken from individuals with inherited mutations in genes involved in DNA replication with DNA from individuals who have normal versions of these genes. The researchers aimed to understand the impact of defective DNA replication on cancer risk and features associated with aging. The results suggest that build-up of mutations in normal cells is unlikely to be the only factor in the development of age-related disease, adding to the ongoing debate about the causes of aging.

Artificial sweeteners are widely promoted as safe, zero-calorie alternatives to sugar, ideal for those trying to lose weight. But a new study is indicating artificial sweeteners may increase appetite and food cravings, particularly in females and the obese.

“There is controversy surrounding the use of artificial sweeteners because a lot of people are using them for weight loss,” says corresponding author on the new study, Kathleen Page. “While some studies suggest they may be helpful, others show they may be contributing to weight gain, type 2 diabetes and other metabolic disorders. Our study looked at different population groups to tease out some of the reasons behind those conflicting results.”

Page hypothesizes the discordancy in the science is somewhat due to the fact that many studies investigating the effects of artificial sweeteners on metabolic activity or the brain are conducted in mostly male subjects, often with normal weight. This new research set out to investigate the influence of artificial sweeteners on these processes across a broad cohort of men and women.

Genetic diseases are a compelling target for viral gene therapy. One condition that scientists are investigating to see if they can treat with gene therapy is a rare genetic disease called Leber congenital amaurosis, or LCA is a progressive condition that disables critical cells within the retina. The damage begins at birth: it eventually robs patients of central vision and color perception, often rendering them legally blind. But there may be another way. On Wednesday, researchers presented evidence from a breakthrough gene-editing experiment that restored some color vision to patients with LCA vision loss.

CRISPR is already under investigation as a gene therapy for blood disorders like sickle cell disease and beta-thalassemia. It may well have other uses, such as treating cancer by editing mutated DNA. But the process is not without its hurdles. Treatments for blood disorders like these involve taking cells from the patient’s body, changing them in vitro in the lab, and then re-infusing them back into the patient’s body. That works great for blood, which you can take out, filter, and put back in with relatively few consequences.

But because LCA is a disease of the retina, you can’t just take out cells and then infuse them back in. The retina is a delicate, multilayered membrane that resents any disturbance. The eye also has a system of physical defenses not unlike the blood-brain barrier. Furthermore, the immune system sometimes responds with extreme prejudice to eye injuries or infections, to the point of causing an actual autoimmune disease where the body attacks its own eyes. How, then, could researchers get the CRISPR treatment into the retina, past the body’s ferocious defenses and without further damage?

(https://www.linkedin.com/in/evelyne-yehudit-bischof/) is an expert in internal medicine and oncology, with a focus on preventative and precision medicine, bio-gerontology, and geronto-oncology.

Dr. Bischof is deeply passionate about next-generation medical technology, and the applications of artificial intelligence for biomedical research and practice.

Continue reading “Dr. Evelyne Bischof, MD — Advancing The Frontiers Of Preventative And Precision Longevity Medicine” »

Fixing breaks in genes with speed and perfection can be a matter of life and death for most organisms. Even the simplest changes in a sequence risk catastrophe, especially if the altered code is responsible for a critical function.

Over the past half a century, biologists have studied the mechanisms involved to piece together most of the major steps involved in making faithful repairs in DNA. Yet, one part of the process has remained frustratingly unclear.

By marking key enzymes and DNA with fluorescent tags and watching the repair process unfold in real-time in an Escherichia coli model, researchers from Uppsala University in Sweden have filled in missing details on how bacteria find the templates they rely on to keep genetic repairs error-free.