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Category: genetics – Page 127

Scientists from the University of Rochester have had the naked mole-rat (Heterocephalus glaber) in their crosshairs for some time, previously identifying how their unique cellular aging mechanisms lay the foundation for their long lifespans – up to 41 years, during which the females also remain fertile – and resistance to age-related diseases.

The modification directly led to the improved overall health of the aging mice and an approximate 4.4% increase in median lifespan.

They weigh about an ounce, spend their lives underground in sub-Saharan Africa and are unlikely to be making the shortlist for any cute animal calendars, but the naked mole-rat continues to show scientists it has incredible age-resistant biology beneath its pale, wrinkly skin.

Building on that knowledge, the researchers genetically modified mice to produce the naked mole-rat version of the hyaluronan synthase 2 gene, which makes a protein that produces high molecular weight hyaluronic acid (HMW-HA). While all mammals have hyaluronan synthase 2, the naked mole-rat’s version is somehow enhanced, driving stronger gene expression.

Continue reading “Naked mole-rat’s ‘longevity’ gene extends lifespan and health of mice” | >

Scientists have found a way to reprogram human cells so that they mimic the highly plastic embryonic stem cells that have so much promise for use in regenerative medicine. By essentially wiping the cell’s “memory”, the team have created so-called induced pluripotent stem (iPS) cells, which could be used to regenerate or repair diseased tissue and organs.

IPS cells are a type of pluripotent cell that can be obtained by reprogramming mature human adult cells (“somatic” cells) into an embryonic stem cell-like state. This means that they have the capacity to differentiate into any cell of the body. They were first demonstrated in 2006, and have myriad potential biomedical and therapeutic uses, including disease modeling, drug screening, and cell-based therapies.

Despite this promise, researchers have continually hit a stumbling block that has prevented iPS cells from realizing their potential. “A persistent problem with the conventional reprograming process is that iPS cells can retain an epigenetic memory of their original somatic state, as well as other epigenetic abnormalities,” Professor Ryan Lister, lead author of a paper presenting the latest breakthrough, said in a statement.

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So past the 7 minute mark we see a competing interest may have stumbled upon the same thing so Katcher and gang are starting a company to commercialize E5.

Here we review a preprint from Dr Katcher and Dr Horvath giving more detail on the experiments which showed a 54% epigenetic rejuvenation in rats and reveals the source of E5 and the processing involved.

Renue By Science 10% : https://tinyurl.com/35jyuk33

Continue reading “The Identity Of E5 Revealed | Reduced Epigenetic Age By More Than 50%” | >

Get my new Longevity Practices book for free: https://www.diamandis.com/longevity.

In this episode, filmed during Abundance360, Peter and David discuss David’s groundbreaking research on reversing aging through epigenetic changes, emphasizing that aging is not just damage to the body but a loss of information. They talk about age reversal as a possibility, rejuvenating brains, and regaining lost memories.

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 Sinclair’s latest study, Chemically Induced Reprogramming to Reverse Cellular Aging: https://www.aging-us.com/article/204896/text.

Continue reading “Aging is Now Optional w/ David Sinclair | EP #60” | >

The origin of the hominines is among the most hotly debated topics in paleoanthropology. The traditional view, ever since Darwin, holds that hominines and hominins originate in Africa, where the earliest hominins are found and where all extant non-human hominines live. More recently a European origin has been proposed, based on the phylogenetic analysis of late Miocene apes from Europe and Central Anatolia1,2,3 The fossils described here attest to a lengthy history of hominines in Europe, with multiple taxa in the eastern Mediterranean known for at least 2.3 Ma4,5,6,7 Our phylogenetic analysis, based on the new specimens described here and a large sample of other fossil and extant hominoids (Supplementary Note 1, Tables 1, 2), supports previous research confirming the hominine status of the eastern Mediterranean apes2,3,8,9,10,11,12,13,14,15,16,17,18,19,20 Our most parsimonious phylogenetic results suggest that hominines in the eastern Mediterranean evolved from dryopithecins in central and western Europe, though there are alternative interpretations21,22,23,24. Either way, the oldest known hominines are European. They may have dispersed into Europe from ancestors in Africa, only to become extinct22 However, the more likely and more parsimonious interpretation is that hominines evolved over a lengthy period in Europe and dispersed into Africa before 7 Ma.

For some time, the only known late Miocene ape from Anatolia was Ankarapithecus, which is alternatively described as a stem hominid or a pongine25,26,27, but not a hominine. It is easily distinguished from Our anopithecus and Graecopithecus from Greece and Bulgaria25,26,27 In 2007, a new species of Our anopithecus was described from Çorakyerler in central Anatolia28. Since then, thousands of vertebrate fossils have been recovered at Çorakyerler, including a well-preserved ape partial cranium29 (Fig. 1) The O. turkae holotype, a fragmented palate, was originally distinguished from O. macedoniensis in its shorter premaxilla, narrower palate, morphologically similar (homomorphic) upper premolars (as opposed to P3 being more triangular than P4), smaller male canines and possibly larger size28. However, recovery of the new cranium and our reanalysis of the published material requires a reassessment of this conclusion and justifies the naming of a new genus of Miocene hominine.

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The viral ALS Ice Bucket Challenge a few years ago raised major funding that resulted in the discovery of new genes connected to the disease. One of those genes is NEK1, in which mutations have been linked to as much as 2% of all ALS cases, making it one of the top-known causes of the disease.

But it wasn’t known how the mutated gene disrupts the function of the motor neuron and causes it to degenerate and die.

Northwestern Medicine scientists have discovered for the first time how this mutated gene leads to ALS (amyotrophic lateral sclerosis).

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A recent study found increased cardiac arrhythmia risk to stay long term in individuals with epilepsy, specially in people who use carbamazepine and valproic acid. The findings of the study were published in European Heart Journal.

Using UK Biobank data, the research also explores the potential roles of genetics and antiseizure medications (ASMs) in this complex relationship. Encompassing 329,432 participants, the study included 2,699 with epilepsy, was initiated between 2006 and 2010. Using advanced statistical techniques like Cox proportional hazards models and competing risk models, the researchers aimed to determine the association between epilepsy history and the incidence of cardiac arrhythmias over an extended period.

Individuals with epilepsy displayed a staggering 36% increased risk of experiencing any form of cardiac arrhythmia compared to those without the condition. This risk extended to specific arrhythmia subtypes, including atrial fibrillation, where a 26% increased risk was identified. More alarmingly, the risk of other cardiac arrhythmias was found to be 56% higher in epilepsy patients.

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For prospective parents who are carriers of many inherited diseases, using in vitro fertilization along with genetic testing would significantly lower health care expenditures, according to researchers at Stanford Medicine.

Preimplantation genetic diagnostic testing during IVF, or PGD-IVF, is being used to screen for single-gene defect conditions such as cystic fibrosis, sickle cell disease and Tay-Sachs disease, along with nearly 400 others.

The problem is that the high cost of IVF — and the lack of coverage by all but one state Medicaid program, that of New York — makes it unavailable to millions of people at risk. The majority of private employer health benefit plans also do not cover IVF.

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This story is part of a series on the current progression in Regenerative Medicine. In 1999, I defined regenerative medicine as the collection of interventions that restore to normal function tissues and organs that have been damaged by disease, injured by trauma, or worn by time. I include a full spectrum of chemical, gene, and protein-based medicines, cell-based therapies, and biomechanical interventions that achieve that goal.

As part of a trio of stories on advances in stem cell gene therapy, this piece discusses how to alter blood stem cells using mRNA technology. Previous installments describe how the same platform could reinvent how we prepare patients for bone marrow transplants and correct pathogenic DNA.

At present, the only way to cure genetic blood disorders such as sickle cell anemia and thalassemia is to reset the immune system with a stem cell transplantation. Only a fraction of patients elects this procedure, as the process is fraught with significant risks, including toxicity and transplant rejection. A preclinical study published in Science explores a solution that may be less toxic yet equally effective: mRNA technology. The cell culture and mouse model experiments offer a compelling avenue for future research to enhance or replace current stem cell transplantations altogether.

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