A review of the most interesting and impactful longevity related studies from December, including how gene therapy can increase telomere length and how the immune system can be used to clear senescent cells.
Contents:
1. Intro 0:00
2. Gene Therapy To Increase Telomere Length 0:48
3. Freeing The Immune System To Remove Senescent Cells 15:20
4. Using Probiotics To Help With Sarcopenia 27:39.
Canadian Content Study.
While the idea of a digital afterlife is fascinating, it raises some big questions. For example, who owns your online accounts after you die?
This issue is already being discussed in courts and by governments around the world. In the United States, nearly all states have passed laws allowing people to include digital accounts in their wills.
In Germany, courts ruled that Facebook had to give a deceased person’s family access to their account, saying that digital accounts should be treated as inheritable property, like a bank account or house.
New research shows somatic mutations drive epigenetic changes tied to aging. This discovery reshapes our understanding of aging and challenges current anti-aging strategies.
Summary: A new study has uncovered a direct link between somatic mutations and epigenetic modifications, challenging established views on aging. Researchers found that random genetic mutations drive predictable changes in DNA methylation, offering new insights into the relationship between mutation accumulation and epigenetic clocks.
This suggests that epigenetic changes may track, rather than cause, aging, making it harder to reverse aging than previously thought. These findings redefine our understanding of aging at the molecular level and hold significant implications for future anti-aging therapies.
Researchers at University of California San Diego School of Medicine have published results that shed new light on an old question: what causes aging at the molecular level? Their findings, published in Nature Aging, describe a never-before-seen link between the two most accepted explanations: random genetic mutations and predictable epigenetic modifications. The latter, also known as the epigenetic clock theory, has been widely used by scientists as a consistent, quantitative measure of biological aging.
However, the new research suggests that the process may not be so simple.
“Major research institutions and companies are betting on turning back the epigenetic clock as a strategy to reverse the effects of aging, but our research suggests that this may only be treating a symptom of aging, not the underlying cause,” said co-corresponding author Trey Ideker, Ph.D., a professor at UC San Diego School of Medicine and UC San Diego Jacobs School of Engineering.
Researchers have found that kinesin family member 9 (KIF9), a protein that diminishes with aging, is instrumental in allowing cells to consume harmful proteins and fights Alzheimer’s in a mouse model.
Consuming amyloids before they become a problem.
Cardiovascular disease continues to lead as the primary cause of death across the globe, taking millions of lives every year. Damage caused by these diseases is particularly difficult to repair, since the heart has minimal ability to regenerate itself. But what if we could reprogram the body’s own cells to restore damaged tissue?
This question has been tackled by scientists at Korea University, led by Dr. Myeong-Hwa Song. The team has unveiled an innovative technique to convert fibroblasts—common connective tissue cells—into mature and functional induced cardiomyocytes (iCMs). Their method relies on combining fibroblast growth factor 4 (FGF4) with vitamin C, a pairing that accelerates cell maturation and enhances function.
“Our findings bring us closer to transforming regenerative medicine into practical therapies,” says Dr. Song, who is based at Korea University’s Department of Cardiology and in Seoul, South Korea. “This research takes an important step toward using a patient’s own cells to repair their heart.”
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OpenAI says it trained a new AI model called GPT-4b micro with Retro Biosciences, a longevity science startup trying to extend the human lifespan by 10 years, according to the MIT Technology Review.
Retro, which is backed by Sam Altman, has been working with OpenAI for roughly a year on this research, according to the report. The GPT-4b micro model tries to re-engineer proteins — a specific set called the Yamanaka factors — that can turn human skin cells into young-seeming stem cells. Retro believes these proteins are a promising step toward building human organs and providing supplies of replacement cells.
The model differs slightly from Google’s Nobel prize-winning AlphaFold, which predicts the shape of proteins, but it appears to be OpenAI’s first model that is custom-built for biological research. OpenAI and Retro tell the MIT Technology Review they plan to release research on the model and its outputs.
Summary: A new study has identified three psychological profiles that influence brain health, cognitive decline, and dementia risk in aging adults. Profiles with high protective traits, like purpose and openness, show better cognition and brain integrity, while those with low protective traits or high negative traits face accelerated brain atrophy and mental health issues.
Researchers emphasize comprehensive psychological assessments to tailor interventions, like therapies that enhance life purpose or reduce distress symptoms. These findings pave the way for personalized strategies to prevent cognitive decline and support brain health in adulthood and aging.
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