At the very start Aubrey claims, so long as he has the funding, he can finish the RMR in 3 years and then things take off from there. He seems to hint that the LEV prediction of 12–15 years could be thrown out and come sooner.
In this in-depth conversation, Dr. Aubrey de Grey discusses his Robust Mouse Rejuvenation (RMR) studies at the LEV Foundation and why he believes we’re close to achieving the crucial RMR milestone within just three years — a breakthrough that could transform aging research forever.
You’ll also hear about: His predictions for reaching Longevity Escape Velocity by the late 2030s. What he would change about Bryan Johnson’s longevity algorithm. How reaching RMR could trigger a global \.
In the context of an ageing world population, certain pathologies that are exacerbated in this process of ageing, such as osteoarthritis (OA), will become more prevalent in the coming years. Moreover, OA is one of the main causes of chronic pain and physical disability in the elderly. It is therefore of great relevance to gain a deep understanding on the pathophysiology of this disease, and also to identify potential prognostic and diagnostic tools along with novel promising therapeutic targets for OA.
New therapies for managing aging could emerge from research into a new gene, which scientists have identified as a key driver of degeneration.
Age-related diseases are strongly linked to inflammation which, when chronic, albeit low-grade, contributes to conditions such as cardiovascular disease, diabetes, neurodegeneration, and sarcopenia, significantly impacting health and longevity.
In a study published in Nature Communications, Dr. Ildus Akhmetov, a geneticist at Liverpool John Moores University’s School of Sport and Exercise Sciences, along with colleagues from Italy, Switzerland, and the Netherlands, uncovered groundbreaking insights into the role of the Ectodysplasin A2 Receptor (EDA2R) in this process.
New therapies for managing ageing could emerge from research into a new gene, which scientists have identified as a key driver of degeneration.
Age-related diseases are strongly linked to inflammation which when chronic, albeit low-grade, contributes to conditions such as cardiovascular disease, diabetes, neurodegeneration, and sarcopenia, significantly impacting health and longevity.
Microbes, Ecology And Medicine — Dr. Sean M. Gibbons, Ph.D. — Associate Professor, Institute for Systems Biology (ISB)
Dr. Sean Gibbons, Ph.D. is Associate Professor at the Institute for Systems Biology (ISB — https://isbscience.org/people/sean-gibbons-phd/?tab=biography where his lab investigates how the structure and composition of evolving ecological networks of microorganisms change across environmental gradients, with a specific focus on how ecological communities in the gut change and adapt to individual people over their lifespans (i.e. host genotype, host development and host behavior) and how these changes impact human health (https://gibbons.isbscience.org/). His lab develops computational and experimental tools for investigating host-associated microbial communities to explore the interactions between ecology, evolution and ecosystem function, applying these insights to develop personalized interventions for improving human health and well-being.
Dr. Gibbons received his PhD in biophysical sciences from the University of Chicago in 2015, dual-advised by Jack Gilbert and Maureen Coleman. His graduate work focused on using microbial communities as empirical models for testing ecological theory.
Dr. Gibbons completed his postdoctoral training in Eric Alm’s laboratory in the Department of Biological Engineering at MIT from 2015–2018. His postdoctoral work focused on developing techniques to quantify individual-specific eco-evolutionary dynamics within the human gut microbiome.
Dr. Gibbons was awarded a Fulbright Graduate Fellowship to study microbiology and synthetic biology at Uppsala University in Sweden, where he earned a master’s degree in 2010. His PhD work was supported by an EPA STAR Graduate Fellowship. Upon joining the ISB faculty in 2018, his startup package was supported, in part, by a Washington Research Foundation Distinguished Investigator Award.
Researchers from Cleveland Clinic’s Genome Center have outlined the pathway human herpes simplex virus-1 (HSV1) can use to contribute to Alzheimer’s disease in aging brains. In a report published in Alzheimer’s & Dementia, investigators also share two FDA-approved, commercially available drugs that reverse this pathway in a laboratory setting.
The findings are the first concrete evidence to support the previously controversial link between human herpesviruses (HHVs) and Alzheimer’s disease. Illustrating the potential for herpes to trigger dementia aids continued efforts to prevent and cure neurodegenerative disease, says senior author and Genome Center director Feixiong Cheng, Ph.D…
For most people, contracting a herpes infection is just an inconvenient or harmless fact of life. Many herpesviruses are individually present in a large percentage of people worldwide, meaning virtually every human being on earth is expected to contract at least three types of herpesviruses by adulthood. Some of these viruses don’t cause symptoms, while others only cause minor illnesses like mono or chickenpox. However, even after these illnesses subside, an infected individual still carries herpesviruses for the rest of their life, with only minor symptoms like occasional cold sores.
Scientists are uncovering the powerful role hormones play in skin aging, revealing new potential treatments for wrinkles, hair graying, and overall skin health.
While traditional anti-aging hormones like retinoids and estrogen have been widely used, new research highlights a broader range of hormones that influence skin structure, pigment, and resilience.
