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Category: genetics – Page 402

A letter was recently published in Nature on 329,000 young people identifying 74 genetic variants—spelling mistakes in single nucleotides in the six billion letter human genome—which can be used to predict nearly 20 percent of the variation in school years completed, a quantitative trait of fortitude which is correlated to general intelligence, and which you can learn about by sequencing your own genome.

Staple that to your college application.

Even before the “molecular age,” we were on guard for the slightest tips that show we are more or less valued than our peers. But there was also caution from the academics that there was actually very little we could do to leverage our biology for improvement. In 1924, the Harvard geneticist William Castle quipped that “we are scarcely as yet in a position to do more than make ourselves ridiculous in this matter. We are no more in a position to control eugenics than the tides of the ocean.”

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Some people live much longer than average, partly thanks to their DNA. A study, published in the European Heart Journal, shows that it could be possible to replicate this genetic gift even for those lacking it. The way is now open to an innovative therapy model capable of preventing and fighting cardiovascular diseases through a real rejuvenation of blood vessels.

The study, conducted by the I.R.C.C.S. Neuromed, the I.R.C.C.S. Multimedica and the Department of Medicine, Surgery, and Dentistry, Salerno Medical School University of Salerno, with the support of the Cariplo Foundation and the Italian Ministry of Health, focuses on the gene that encodes the BPIFB4 . In the past, the same research group had identified a variant of this gene, the so-called LAV (“longevity associated variant”), which prevails in people over 100 years of age. Now, through a , researchers have inserted the LAV-BPIFB4 gene into the DNA of animal models particularly susceptible to atherosclerosis and, consequently, to cardiovascular diseases.

“The results—says Annibale Puca, coordinator of a research team at the University of Salerno and at I.R.C.C. MultiMedica—were extremely encouraging. We observed an improvement in the functionality of the endothelium (the inner surface of blood vessels), a reduction of atherosclerotic plaques in the arteries and a decrease in the inflammatory state.”

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For a core of longevity true believers, the time to intervene is now.

“How old are you?” James Clement wanted to know.

I turn 50 this year. There’s a new creaking in my bones; my skin doesn’t snap back the way it used to. It’s developed a dull thickness—you can’t tickle me at all. My gums are packing it in and retreating toward my jaw. These changes have been gradual or inexplicably sudden, like the day when I could no longer see the typed words that are my profession. Presbyopia, the ophthalmologist told me. Totally normal. You’re middle-aged.

To Clement, though, my age was great news. “Yep, you are going to live forever,” he said. “I think anybody under 50 who does not have a genetic liability will make it to longevity escape velocity.”

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A team of scientists at UC San Francisco and the National Institutes of Health have achieved another CRISPR first, one which may fundamentally alter the way scientists study brain diseases.

In a paper published August 15 in the journal Neuron, the researchers describe a technique that uses a special version of CRISPR developed at UCSF to systematically alter the activity of in human neurons generated from , the first successful merger of stem cell-derived cell types and CRISPR screening technologies.

Though mutations and other genetic variants are known to be associated with an increased risk for many , technological bottlenecks have thwarted the efforts of scientists working to understand exactly how these genes cause .

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A new study outlines multiple ways in which epiblast stem cells can be reprogrammed back into a fully pluripotent state, paving the way for a better understanding of epigenetics.

The role of epigenetics

Epigenetics are why our cells, which all have the same DNA, differ in function. A bone cell has the same genetics as a nerve cell, but its epigenetic switches instruct it to perform the functions of a bone cell and not a nerve cell. Epigenetic alterations, however, are one of the primary hallmarks of aging. As we age, harmful epigenetic switches are activated and beneficial ones are deactivated, causing age-related dysfunction. This may even lead to inflammation, which causes further epigenetic damage, leading to a dangerous feedback loop.

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A research group at ETH Zurich, Switzerland, has made it possible to edit hundreds of genes at once with CRISPR gene editing.

CRISPR gene editing has revolutionized the biotech industry by providing an easy and quick way to genetically modify organisms. So far, however, CRISPR techniques have only managed to edit a maximum of seven genes at once. This limits the potential of the technique in creating cell therapies, since whole networks of genes need to be reprogrammed to control each cell’s fate.

The Swiss research group devised a way to overcome this limitation with a CRISPR technique able to edit 25 genes in one go. This number could also be increased to up to hundreds of genes at a time. This method therefore makes it possible to edit gene networks, and reprogram stem cells to become cell therapies such as skin cells or insulin-producing pancreatic cells.

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Dr. Michael West, CEO of AgeX Therapeutics and Founder of Geron Corporation, discusses breakthroughs in the understanding of biological regeneration and in induced tissue regeneration, through his talk “Hayflick Rewound: Somatic Restriction, Epigenetics, and the Reversibility of Human Aging”. This talk was given at the Ending Age-Related Diseases conference in NYC. Join us at http://lifespan.io/hero

►Conference Page: https://www.leafscience.org/ending-age-related-diseases-adva…prospects/
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►This video is presented by LEAF. Please support our work by becoming a “Lifespan Hero”: http://lifespan.io/hero

► #LifeExtension #MichaelWest #AgeX

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