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We will be returning in 2020 to host our third conference in New York City and brings together the leading experts in aging research and biotech business and investment. Building on the success of our 2018 and 2019 conferences we will continue to bring you the latest research, business, and investment talks from some of the top leaders in their fields.

We will be releasing more information about the conference in the coming months as we confirm speakers, venue, and dates. If you would like to stay informed about developments and ticket offers you may wish to sign up for the conference mailing list below.

Approves the First Disposable €˜Scope €™- via The New York Times #perpetuallife

https://www.nytimes.com/2019/12/13/health/disposable-duodeno…tions.html

Reusable duodenoscopes infected patients in a series of notorious outbreaks. Now there €™s a disposable model to be used just once.

Chemotherapy is a powerful weapon in the fight against cancer, but the complex nature of the disease means that it doesn’t always produce the desired result. Scientists at the Salk Institute have been researching some of the cellular processes behind these evasive abilities, uncovering a new mechanism that could pave the way for new treatments that see chemotherapy maintain the upper hand.

The work was carried out at the Salk Institute’s Molecular and Cell Biology Laboratory, where medical scientists led by Gerry Shadel set out to investigate the role mitochondria might play in the effectiveness of chemotherapy.

Mitochondria is best known as the power generator of the vast majority of cells, but the scientists have found that it can also act as an early warning sign when something’s not quite right. While most of the DNA we carry is packed inside the nucleus of the cell, mitochondria packs its own small set of DNA, called mtDNA.

Taking advantage of powerful advances in CRISPR gene editing, scientists at the University of California San Diego have set their sights on one of society’s most formidable threats to human health.

A research team led by Andrés Valderrama at UC San Diego School of Medicine and Surashree Kulkarni of the Division of Biological Sciences has developed a new CRISPR-based gene-drive system that dramatically increases the efficiency of inactivating a gene rendering bacteria antibiotic-resistant. The new system leverages technology developed by UC San Diego biologists in insects and mammals that biases genetic inheritance of preferred traits called “active genetics.” The new “pro-active” genetic system, or Pro-AG, is detailed in a paper published December 16 in Nature Communications.

Widespread prescriptions of antibiotics and use in animal food production have led to a rising prevalence of antimicrobial resistance in the environment. Evidence indicates that these environmental sources of antibiotic resistance are transmitted to humans and contribute to the current health crisis associated with the dramatic rise in drug-resistant microbes. Health experts predict that threats from antibiotic resistance could drastically increase in the coming decades, leading to some 10 million drug-resistant disease deaths per year by 2050 if left unchecked.

The National Institutes of Health (NIH) estimates that in 2018, over 10 million teens and adults misused opioids. The prescription of opioids to treat patient pain is one of many factors contributing to this epidemic; to solve it, a multipronged approach is needed.

Two new Mayo Clinic studies — one in clinical practice and one in the laboratory — could offer new solutions to help patients manage pain without the use of opioids. These projects have been singled out for federal funding under the NIH’s Helping to End Addiction Long-Term (HEAL) Initiative, a multimillion dollar, multiorganizational approach to providing pain-treatment alternatives and turning the tide on the opioid crisis.

“Opioids remain one part of the continuum of pain treatment,” says Andrea Cheville, M.D., a rehabilitation physician at Mayo and member of the National Academy of Medicine. “There are other options that work as well, or better in some cases, with fewer risks. Our new research mirrors a broad Mayo priority — finding the safest, most effective way to help our patients manage acute or chronic pain.”

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.

Continue reading “Dr. David Sinclair Webinar – Lifespan: Why We Age – and Why We Don’t Have To” »

Drugs can cause permanent harm to the brain. We’re only beginning to find ways to heal the hurt.

Scientists from the Salk Institute for Biological Studies are homing in on exactly how two new experimental Alzheimer’s drugs could be generating the anti-aging effects seen in early animal studies. The discovery of a unique metabolic pathway, associated with both general aging and the onset of dementia, offers researchers novel directions for future anti-aging studies.

Salk researchers have been developing two experimental drugs for several years with a view on improving cognition and slowing the neurodegenerative decline associated with Alzheimer’s disease. Called CMS121 and J147, the drugs were effective in slowing the progression of Alzheimer’s in initial animal tests. However, the compounds also seemed to demonstrate signs of slowing down general markers of brain aging.

As the two drugs move toward human trials, the researchers have been working to uncover exactly what molecular mechanisms are at play to explain how they work. One potential mechanism was uncovered in early 2018 but that was only part of the story. Now, the Salk team has uncovered an exciting new molecular pathway, influenced by the two drugs, that could explain how the compounds slow down brain aging.