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Our DNA is made up of genes that vary drastically in size. In humans, genes can be as short as a few hundred molecules known as bases or as long as two million bases. These genes carry instructions for constructing proteins and other information crucial to keeping the body running. Now a new study suggests that longer genes become less active than shorter genes as we grow older. And understanding this phenomenon could reveal new ways of countering the aging process.

Luís Amaral, a professor of chemical and biological engineering at Northwestern University, says he and his colleagues did not initially set out to examine gene length. Some of Amaral’s collaborators at Northwestern had been trying to pinpoint alterations in gene expression—the process through which the information in a piece of DNA is used to form a functional product, such as a protein or piece of genetic material called RNA—as mice aged. But they were struggling to identify consistent changes. “It seemed like almost everything was random,” Amaral says.

Then, at the suggestion of Thomas Stoeger, a postdoctoral scholar In Amaral’s lab, the team decided to consider shifts in gene length. Prior studies had hinted that there might be such a large-scale change in gene activity with age—showing, for example, that the amount of RNA declines over time and that disruptions to transcription (the process through which RNA copies, or transcripts, are formed from DNA templates) can have a greater impact on longer genes than shorter ones.

Many neurodegenerative diseases, including Alzheimer’s.

Alzheimer’s disease is a disease that attacks the brain, causing a decline in mental ability that worsens over time. It is the most common form of dementia and accounts for 60 to 80 percent of dementia cases. There is no current cure for Alzheimer’s disease, but there are medications that can help ease the symptoms.

Let me assure you that my intent in this article is not to refute any empirical data or established theories about telomeres. Instead, I will explain why I believe that the historical course of scientific discoveries and an outdated paradigm about the biological cause of aging have led to the use of inaccurate language in describing the roles and functions of telomeres.

Aubrey De Grey discusses the progress and potential of therapies related to his ideas on anti-aging medicine, including the four therapies that will be tested in a mouse rejuvenation trial. He also shares his thoughts on partnering with organizations and individuals in the field, integrating AI into his work, and the importance of structure in maximizing impact. Aubrey de Grey discusses the potential for Yamanaka factors to be used in organ rejuvenation, and the role of transcription factors in creating induced pluripotent stem cells. He also provides advice for those interested in getting involved in the field and shares his views on time management and productivity. Aubrey De Grey discusses the potential for reversing the pathology of aging to address mechanical issues and mentions promising research being conducted by MAIA Biotechnology on cancerous cells that express telomerase. He also expresses his optimism about the possibility of reaching “longevity escape velocity” within the next 15 years.

Youtube:
Aubrey De Grey links.
https://twitter.com/aubreydegrey?ref_src=twsrc%5Egoogle%7Ctw…r%5Eauthor.
https://www.levf.org/
https://www.linkedin.com/in/aubrey-de-grey-24260b/

PODCAST INFO:
The Learning With Lowell show is a series for the everyday mammal. In this show we’ll learn about leadership, science, and people building their change into the world. The goal is to dig deeply into people who most of us wouldn’t normally ever get to hear. The Host of the show – Lowell Thompson-is a lifelong autodidact, serial problem solver, and founder of startups.
LINKS
Youtube: https://www.youtube.com/channel/UCzri06unR-lMXbl6sqWP_-Q
Youtube clips: https://www.youtube.com/channel/UC-B5x371AzTGgK-_q3U_KfA
Linkedin: https://www.linkedin.com/in/lowell-thompson-2227b074
Twitter: https://twitter.com/LWThompson5
Website: https://www.learningwithlowell.com/
Podcast email: [email protected].
Timestamps.
00:00 Start.
01:00 Mark Hamaleinen write in question: Why we still don’t have any therapies based on his ideas published 20 years ago in his breakout paper.
04:30 update on escape velocity. 50% in 15 years.
08:30 Experiments on mice.
12:00 Yamanaka factor thoughts, current research on mice continued.
14:30 Lev foundation research expanded and explained.
16:30 Lev foundation thesis compared to others.
21:00 Hardships being at the tip of the innovation field of longevity.
23:45 Open source, non profits, lev foundation.
26:00 Ideas from previous organizations (ie. SENS) applied in LEV
27:15 Ichor therapeutics, and partnership process of LEV
29:30 Next generation mentorship.
30:30 Summer internship program.
32:45 Bullish on longevity.
33:30 AI role in longevity.
35:55 Anything fundamental making longevity therapies only for the rich.
38:30 Longevity surgery therapies.
39:30 Advice for people.
40:30 Bottlenecks of longevity.
42:00 Books!
43:05 Staying on cutting edge/ learning.
44:15 Current curiosity and fascination.
46:45 What happiness means to him and how he optimizes for it.
48:30 how he stays healthy over the years, longevity practices he uses.
51:45 How much money does he and the space need.
52:55 Anything stopping him from getting Jeff Bezos and other high network people to invest or donate.
51:55 Thoughts on altos labs & calico labs.
56:35 up and coming people that inspire him (crypto people, michael levin)
59:00 Finding up and coming people to work with and for (advice)
60:30 Things people get wrong and what people ask him about longevity.
1:01:35 Aubrey newsletter and updates (news suggestions)
1:03:30 Question he wonders about that doesn’t have answer to.
1:04:15 How he maximizes his day and stays productive.
1:05:15 Thoughts on MAIA Biotechnology, telomerase, short vs long.
1:09:30 Final thoughts on lev foundation.

#longevity #aubreydegrey #LEVF

People age at different rates due to a variety of intrinsic and extrinsic factors, which can affect their biological age and their risk of developing diseases or experiencing early death. This is why two individuals who are both 50 years old may not have the same level of biological aging, despite having lived for the same number of years.

Lifestyle choices, such as diet and smoking, and illness all contribute to accelerating biological age beyond one’s chronological age. Researchers have discovered that grip strength, a measure of overall muscle strength, is linked to biological age in this way. In particular, the study, which was published in the Journal of Cachexia, Sarcopenia, and Muscle, found that people with weaker grip strength had older biological ages.

Researchers at Michigan Medicine modeled the relationship between biological age and grip strength of 1,274 middle-aged and older adults using three “age acceleration clocks” based on DNA.

This week our guest is business and technology reporter, Peter Ward. Earlier this year, Peter released his book The Price of Immortality: The Race to Live Forever, where he investigates the many movements and organizations that are seeking to extend human life, from the Church of Perpetual Life in Florida, to some of the biggest tech giants in Silicon Valley.

In this episode, we explore Peter’s findings, which takes us on a tour from cryonics to mind uploading, from supplements to gene editing, and much more. Along the way, we discuss the details of how one might actually achieve immortality, the details of senescent cells and telomeres, whether it’s better to live healthy than to live long, the scams and failures that seem to dominate the space, as well as the efforts that seem most promising.

Find Peter’s work on PenguinRandomHouse.com or follow him at twitter.com/PeterWardJourno.

Host: steven parton — linkedin / twitter.

Nuclear morphology changes with aging, but the role of these changes and the underlying mechanisms are not fully understood. The authors find that the nuclear envelope anchor protein ANC-1 in worms, and its counterpart nesprin-1 and nesprin-2 in mammals, promotes the degradation of nuclear components to limit nucleolar size and function in a soma longevity and germline immortality mechanism.

She cooks, she cleans, and she still finds time to play ball with Elroy,” George and Jane Jetsons’ six-and-a-half-year-old son. Set in the year 2062 and described in the 1960s animated sitcom The Jetsons as an “aluminum-encased, battery-powered robotic maid” who is the “perfect answer for any modern family,” Rosie the Robot takes care of chores around the house while also serving as friend and confidante of mother Jane. Sarcastic and funny, Rosie is a hardworking nanny and aunt figure to children Elroy and Judy.

While many technologies The Jetsons predicted for 2062 have become reality, such as video calls and smart watches, the full realization of robots as the 1960s ideal friend and helper who makes life easier has yet to be fulfilled. For twenty-five years, roboticist Daniel Theobald has been on a mission to create robots that can solve the world’s most pressing problems. But rather than focus solely on making robots be more human, his calling has been to use them to help humans be more human.

The co-founder of Vecna Technologies and Vecna Robotics tells the story of a client who once came to him worried about their aging population. Vecna was one of the only modern robotics companies doing cutting edge work, and they wanted to talk about creating robots to take care of the elderly. Theobald says, “I felt that was completely backwards. Why would we build robots to take care of humans, and send our humans to work in a factory? Robots should be used to do the things that don’t matter. People need real, meaningful work like taking care of each other and the people we love. We should use technology to give us more time to be human, to do more meaningful activities like art, science, caring for the elderly, exploration of the universe, those sorts of things.”

Ray Kurzweil, an American Jewish inventor and futurist, claims that within ten years, man will be able to defeat old age and death thanks to the accelerated development of technology.

My question in relation to Kurzweil’s statement is: What is so good about us constantly living all the time? Why live at all if we are never to die?

On the contrary, if we attain the purpose of our lives while we are alive, then we will reach a spiritual, eternal, and perfect state, i.e. one where we will have no feeling of a lack. In our current lives, we constantly live out of feeling lack and the need to fulfill our lacks. However, we can reach a state where we have no such feeling of a lack, but that we have an abundance of everything.

Developing ourselves spiritually has nothing to do with medicine or technology. It has to do with our inner world, i.e. with how we feel that we can give and receive from everyone, and live in a world that is boundless, with no beginning or end. Then, even if our bodies die, we will not feel it as death.

In this episode, David and Peter discuss aging as a disease, the technology needed to reverse aging, and tips and tricks to increase your lifespan.

David Sinclair is a biologist and academic known for his expertise in aging and epigenetics. Sinclair is a genetics professor and the Co-Director of Harvard Medical School’s Paul F. Glenn Center for Biology of Aging Research. He’s been included in Time100 as one of the 100 Most Influential People in the World, and his research has been featured all over the media. Besides writing a New York Times Best Seller, David has co-founded several biotech companies, a science publication called Aging, and is an inventor of 35 patents.
Read David’s book, Lifespan: Why We Age-and Why We Don’t Have To: https://a.co/d/85H3Mll.

This episode is brought to you by Levels: real-time feedback on how diet impacts your health. https://levels.link/peter.

Consider a journey to optimize your mind and body by visiting http://mylifeforce.com/peter.