Lifeboat Foundation

With billions of dollars flooding into longevity, what role will epigenetic clocks play in measuring and intervening in aging?

When Horvath first described epigenetic clocks, scientists began to speculate that altering them could reverse aging. After all, if certain patterns of DNA methylation at certain sites in cells in certain tissues of your body are hallmarks of aging, could shifting them somehow reverse aging?

More than six months after CAR-T cell treatment, five patients are in remission and have functional immune systems.

Optimizing Human-System Performance — Dr. Greg Lieberman, Ph.D., Neuroscientist / Lead, U.S. Army Combat Capabilities Development Command Army Research Laboratory, U.S. Army Futures Command

Dr. Greg Lieberman, Ph.D. (https://www.arl.army.mil/arl25/meet-arl.php?gregory_lieberman) is a Neuroscientist, and Lead, Optimizing Human-System Performance, at the U.S. Army Combat Capabilities Development Command, Army Research Laboratory (DEVCOM ARL).

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In nature, evolutionary chromosomal changes may take a million years, but scientists have recently reported a novel technique for programmable chromosome fusion that has successfully created mice with genetic changes that occur on a million-year evolutionary scale in the laboratory. The findings might shed light on how chromosomal rearrangements – the neat bundles of structured genes provided in equal numbers by each parent, which align and trade or mix characteristics to produce offspring – impact evolution.

In a study published in the journal Science, the researchers show that chromosome level engineering is possible in mammals. They successfully created a laboratory house mouse with a novel and sustainable karyotype, offering crucial insight into how chromosome rearrangements may influence evolution.

“The laboratory house mouse has maintained a standard 40-chromosome karyotype — or the full picture of an organism’s chromosomes — after more than 100 years of artificial breeding,” said co-first author Li Zhikun, researcher in the Chinese Academy of Sciences (CAS) Institute of Zoology and the State Key Laboratory of Stem Cell and Reproductive Biology. “Over longer time scales, however, karyotype changes caused by chromosome rearrangements are common. Rodents have 3.2 to 3.5 rearrangements per million years, whereas primates have 1.6.”

Biotech start-up Pretzel Therapeutics launched Monday with $72.5 million in Series A financing to develop novel, mitochondria-based therapies for rare genetic disorders and diseases of aging.

Pretzel plans to target mitochondrial diseases, a highly heterogenous group of conditions caused by DNA mutations in the mitochondria or the nucleus. These disorders are very rare, afflicting around one in 5,000 people.

Pretzel CEO Jay Parrish told BioSpace the funding “should enable us to get close to the clinic if not into the clinic with one or more programs.”

You won’t be able to blame it on your genetics anymore: with CRISPR, it’s so easy to hacn into your DNA. CRISPR technology is our future, and experiments with DNA hacking are booming. CRISPR biotechnology is not science fiction anymore, it is our very near future. Would you hack and reprogram your own DNA with CRISPR? Breaking the code of life, hacking DNA at home.

Welcome to the world of a new nature. We can now literally cut and paste DNA with the new CRISPR technology. There is a revolutionary development going on that will have major consequences for humans, plants and animals. The new biotechnology is here.

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U.S. regulators have approved a new purple tomato, genetically engineered to be packed with antioxidants and anthocyanins. The fruit will go on sale in 2023.

(Medical Xpress)—A team of researchers at the Max Planck Institute has found what they believe is the DNA mutation that led to a change in function of a gene in humans that sparked the growth of a larger neocortex. In their paper published in the journal Science Advances, the team describes how they engineered a gene found only in humans, Denisovans and Neanderthals to look like a precursor to reveal its neuroproliferative effect.

A year ago, another team of researchers found the human gene that most in the field believe was a major factor in allowing the human brain to grow bigger, allowing for more complex processing. In this new effort, the researchers have found what they believe was the DNA change that arose in that gene.

To pinpoint that change, the researchers engineered the unique ARHGAP11B gene to make it more similar to the ARHGAP11A gene, which researchers believe was a predecessor gene—they swapped a single nucleotide (out of 55 possibilities) for another and in so doing, found the ARHGAP11B gene lost its neuroproliferative abilities. This, the team claims, shows that it was a single mutation that allowed humans to grow bigger brains. Such a mutation, they note, was not likely due to natural selection, but was more likely a simple mistake that occurred as a brain cell was splitting. Because it conferred an advantage (the ability to grow higher than normal amounts of brain cells) the mutation was retained through subsequent generations. They also point out that such a mutation would have resulted specifically in a larger neocortex—a portion of the cortex that has been associated with hearing and sight.

When the right gene is expressed in the right manner in the right population of stem cells, the developing mouse brain can exhibit primate-like features. In a paper publishing August 7th in the Open Access journal PLOS Biology, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) succeeded in mimicking the sustained expression of the transcription factor Pax6 as seen in the developing human brain, in mouse cortical progenitor cells. This altered the behavior of these cells to one that is akin to that of progenitors in the developing primate neocortex. Consequently, the mouse progenitors generated more neurons — a prerequisite for a bigger brain.

The neocortex consists of different types of progenitors, but one particular class, the basal progenitors, behave differently in small-brained animals such as mice than in large-brained animals such as humans. In humans, basal progenitors can undergo multiple rounds of cell division, thereby substantially increasing neuron number and ultimately the size of the neocortex. In mice, these progenitors typically undergo only one round of cell division, thus limiting the number of neurons produced. A potential cause underlying this difference in the proliferative capacity of basal progenitors could be the differential expression of Pax6 between species. Mouse basal progenitors, in contrast to human, do not express Pax6. “We were very curious to see what would happen if we were to change the expression pattern of Pax6 in developing mouse brain to mimic that observed in large-brained animals”, says Fong Kuan Wong, a PhD student in the lab of Wieland Huttner and first author of the study.

To this end, another PhD student in the lab, Ji-Feng Fei, generated a novel transgenic mouse line. This line provided the basis for altering the expression of Pax6 in the cortical stem cell lineage such that it would be sustained in basal progenitors. The researchers then introduced the Pax6 gene into the stem cells of these mice. Strikingly, sustaining Pax6 expression in mouse basal progenitors increased their capacity to undergo multiple rounds of cell division, as typically observed in primates. This not only expanded the size of the basal progenitor population in a way somewhat reminiscent to what is seen in large-brained animals. It also resulted in an increase in cortical neurons, notably those in the top layer, another characteristic feature of an expanded neocortex.