A recent study has found that the overexpression of telomerase reverse transcriptase (TERT), which is a subunit of telomerase, an enzyme essential for telomere maintenance, leads to lifespan extension in mice without significant side effects [1].
Protecting DNA
Telomere shortening is a well-known hallmark of aging. Telomeres are protective DNA sequences at the ends of the chromosomes. In most human cells, they become shorter with each division.
NAD, a vital molecule for cellular energy and DNA
DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).
Researchers at the University of Colorado Anschutz Medical Campus have found a promising drug candidate that could help restore vision in individuals with multiple sclerosis (MS) and other neurological conditions that damage neurons.
The study was published this week in the journal Nature Communications.
The drug, LL-341070, enhances the brain’s ability to repair damaged myelin — the protective sheath around nerve fibers. Damage to myelin is a hallmark of diseases like MS, as well as a natural consequence of aging, often resulting in vision loss, loss of motor skills, and cognitive decline.
Genetic engineering is a beacon of hope. It promises eternal life, curing diseases and feeding the growing world population. The possibilities are boundless. The invention is not that old. But their pace is rapid. Life without genetic engineering will no longer exist. We are at the beginning of a new evolution.
The Silent Front (Extra Long Documentary) — • The Silent Front: Spies and Secrets o…
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Welcome to the official Get.factual youtube channel! 🌍
We are a documentary streaming channel covering history, science, technology, and nature. Explore worlds distant, forgotten, and unknown; from the depths of ocean trenches to the far reaches of the cosmos.
LEV is upon us.
OpenAI chief executive Sam Altman, who provided the initial $180mn to seed the start-up, will put in more money in the series A. The company is in talks with family offices, venture capitalists and sovereign wealth funds, as well as a US “hyperscaler” data centre to provide computing power to run the AI models it uses to create and test its treatments.
In partnership with OpenAI, the start-up has built a bespoke AI model that designs proteins to temporarily turn regular cells into stem cells, which it says can reverse their ageing process.
The San Francisco-based biotech will use the money to fund clinical trials for three drugs, including a potential treatment for Alzheimer’s disease, which will be tested in an early stage study in Australia this year. It is also working on drugs for rejuvenating blood and brain cells.
LEV is upon us.
OpenAI chief executive Sam Altman, who provided the initial $180mn to seed the start-up, will put in more money in the series A. The company is in talks with family offices, venture capitalists and sovereign wealth funds, as well as a US “hyperscaler” data centre to provide computing power to run the AI models it uses to create and test its treatments.
In partnership with OpenAI, the start-up has built a bespoke AI model that designs proteins to temporarily turn regular cells into stem cells, which it says can reverse their ageing process.
The San Francisco-based biotech will use the money to fund clinical trials for three drugs, including a potential treatment for Alzheimer’s disease, which will be tested in an early stage study in Australia this year. It is also working on drugs for rejuvenating blood and brain cells.bn for project to extend human life” | >
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.
