Building on their groundbreaking research in epigenetics and transposable elements related to aging, scientists at Eötvös Loránd University have achieved a significant breakthrough in unraveling the molecular mechanisms of aging.
Drs. Ádám Sturm and Tibor Vellai of Eötvös Loránd University have achieved another significant breakthrough in the study of aging, expanding on their groundbreaking research into the epigenetics of aging and transposable elements. These new findings have deepened our understanding of the molecular mechanisms behind aging.
Their latest study, published in the International Journal of Molecular Sciences, reveals a novel epigenetic mechanism in mitochondrial DNA (mtDNA) that could revolutionize our approach to aging research and diagnostics.
In their previous landmark articles, “The mechanism of aging: primary role of transposable elements in genome disintegration” (2015) and “Downregulation of transposable elements extends lifespan in Caenorhabditis elegans” (2023), Dr. Sturm and Dr. Vellai established the crucial role of transposable elements in the aging process. Their current research expands on this foundation, uncovering a new layer of complexity in cellular aging.
Discovery of the Mitochondrial Epigenetic Clock
The research team has discovered that a previously hidden DNA modification, N6-methyladenine (6mA), that progressively accumulates in mtDNA as organisms age. This phenomenon was observed across diverse species, including the nematode Caenorhabditis elegans, the fruit flyDrosophila melanogaster, and dogs, suggesting an evolutionary conserved mechanism in the aging process across all animal species.
“We’ve discovered what could be described as a ‘mitochondrial epigenetic clock,” explains Dr. Sturm. “This clock ticks at different rates depending on the lifespan of the organism, providing a new perspective on how aging is regulated at the cellular level. It’s fascinating to see how this connects to our earlier work on transposable elements and genome stability.”
To resolve earlier disputes about the existence of the hidden 6mA modification mark in animal genomes, the team developed a novel, reliable PCR-based method for detecting these modifications. This technique allows for accurate, sequence-specific measurement of 6mA levels in mtDNA, overcoming the limitations of previous methods.
Linking 6mA Accumulation to Longevity
A key finding of the study was that long-lived C. elegans mutants, which live twice as long as wild-type worms, accumulate 6mA at half the rate of their normal counterparts. This observation strongly links the rate of 6mA accumulation to the aging process and lifespan regulation, reminiscent of the team’s earlier findings on transposable element activity and longevity.
The research also elucidated the enzymatic pathways responsible for adding and removing 6mA modifications in mtDNA. Surprisingly, these appear to be the same enzymes involved in nuclear DNA methylation, suggesting a coordinated epigenetic regulation across different cellular compartments.
Dr. Vellai emphasizes the potential implications of this discovery: “Our findings open up new avenues for understanding and potentially intervening in the aging process. This epigenetic clock in mtDNA could serve as a more accessible and cost-effective way to measure biological age, compared to existing methods. When combined with our previous insights on transposable elements, we’re gaining a more comprehensive picture of the aging process.”
The study paves the way for future research on how environmental factors, lifestyle choices, and potential interventions might influence the rate of 6mA accumulation in mtDNA and transposable element activity. Understanding these epigenetic changes could lead to novel strategies for promoting healthier aging and potentially extending healthspan.
Reference: “N6-Methyladenine Progressively Accumulates in Mitochondrial DNA during Aging” by Ádám Sturm, Himani Sharma, Ferenc Bodnár, Maryam Aslam, Tibor Kovács, Ákos Németh, Bernadette Hotzi, Viktor Billes, Tímea Sigmond, Kitti Tátrai, Balázs Egyed, Blanka Téglás-Huszár, Gitta Schlosser, Nikolaos Charmpilas, Christina Ploumi, András Perczel, Nektarios Tavernarakis and Tibor Vellai, 2 October 2023, International Journal of Molecular Sciences.
DOI: 10.3390/ijms241914858
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10 Comments
Having found documentation years ago that allergies, a source of inflammation, and gout (a high serum level of uric acid), a product of inflammation, go back millennia in human history, I hope this new information will help to determine and remedy it that the average human lifespan in 2024 is much shorter than it should be, that humanity needs more affordable, convenient and reliable means for identifying an individual’s nearly subclinical non-IgE-mediated food allergies (e.g., Dr. Arthur F. Coca, by 1935) and that toxic officially (FDA in the US) food additives play a major role in turning practically harmless individual very, very mild food allergy reactions into chronic, deadly dangerous and life shortening ones, long-term (months to decades; highly individual; many individual variables).
Gates, Fauci, and the gang don’t want us to live longer. They want to kill us.
Rufus. You are an idiot.
Rufus. You are an idiot. Go back to MAGA-Cult land…
Bob, Nicholas, Rufus may be partly right. Statistically, about 75% of US mortality is premature due to cheaply and easily prevented chronic diseases. It may be an ‘unintended consequence’ of the ‘ruling allergy ignorant’ to cause another 6,000 (my estimate) Americans to die prematurely today (e.g., about 30 million of us just since 1980; soy, TBHQ and MSG, minimally) when what they probably want is to profit from their externally imposed illnesses, indefinitely. One serious concern of mine is what if the next unintended consequence is a true global pandemic or the early extinction of our entire species? Every toxic new officially (FDA in the US) approved food additive is potentially a ‘home grown’ mass extinction meteor.
“The team developed a novel, reliable PCR-based method for detecting these modifications. This technique allows for accurate, sequence-specific measurement of 6mA levels in mtDNA, overcoming the limitations of previous methods.” That is what this study is about. It’s not about aging, per se. They only looked at one worm species, fruit flies, and dogs. This found a correlation, no causation, between mitochondrial DNA 6mA levels and aging.
The study is a demonstration of their newly patented technique. According to the actual study, linked to at the end of the article above, is the statement: “Conflicts of Interest — The authors declare the following competing interests: related patent applications include P2100409, W2200015, P2200206 and W2200017. Vellab Biotech Ltd. is a project company that was established in 2019 by several scientists with the consent of Eötvös Loránd University to develop a method by which age can be determined from DNA.”
So this is a sales pitch, not a breakthrough. People have been selling hope for anti-aging since people have been dying. It’s the second oldest profession selling a Fountain of Youth.
“aging process. This epigenetic clock in mtDNA could serve as a more accessible and cost-effective way to measure biological age, compared to existing methods. “ There’s the real pitch. Use their method to check your mitochondria for signs of how old you are. I’m sure they hope to sell home test kits, so people can check daily to see how they are aging. Unfortunately, this tells you nothing useful, or how to better live your life to stay healthy and possibly live longer. But one way to live longer is to stop worrying about living longer, which is stressful and leads people to do ridiculous things, like take tests for their mitochondrial DNA 6mA levels.
Good luck
Interesting, but, even with some good science, the genetic pre set of 120 years is not evolutionary nor modifiable by man. The age of 120 years has been known to man for over 7000 years. Research seems redundant and a waste of resources.
What would you say is the 1st oldest profession?
For their next project, perhaps those scientists can answer the question, “How do we make a world in which people actually want to live longer?”