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Muscle from a mouse model of Duchenne muscular dystrophy. Fibrous scar tissue is in blue and healthy muscle is in pink. CONBOY LAB AND MURTHY LAB While promising, applications of CRISPR-Cas9 gene editing have so far been limited by the challenges of delivery—namely, how to get all the CRISPR parts to every cell that needs them. In a study published today (October 2) in Nature Biomedical Engineering, researchers have successfully repaired a mutation in the gene for dystrophin in a mouse model of Duchenne muscular dystrophy by injecting a vehicle they call CRISPR-Gold, which contains the Cas9 protein, guide RNA, and donor DNA, all wrapped around a tiny gold ball.

The authors have made “great progress in the gene editing area,” says Tufts University biomedical engineer Qiaobing Xu, who did not participate in the work but penned an accompanying commentary. Because their approach is nonviral, Xu explains, it will minimize the potential off-target effects that result from constant Cas9 activity, which occurs when users deliver the Cas9 template with a viral vector.

Duchenne muscular dystrophy is a degenerative disease of the muscles caused by a lack of the protein dystrophin. In about a third of patients, the gene for dystrophin has small deletions or single base mutations that render it nonfunctional, which makes this gene an excellent candidate for gene editing. Researchers have previously used viral delivery of CRISPR-Cas9 components to delete the mutated exon and achieve clinical improvements in mouse models of the disease.

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Leading women’s magazine Marie Claire has a feature story on life extension out this month (approx 1.5 million circulation):


Forget about life after death. More and more, women around the country are seeking another kind of miracle: not dying at all.

What if you could hit the pause button on aging? Live to 120 without feeling a day over 80? More radical still, what if you could cheat death? Would you do it?

“Life extensionists” would. That’s the name modern immortality seekers now go by, and devotees range from those who’d like to live healthier lives into old age to the more extreme, who ardently believe that humans can, and should, overcome death the same way we’ve overcome, say, smallpox or tooth decay.

Chinese scientists used an adapted version of a controversial gene-editing technique to correct a disease-causing mutation in human embryos, a medical first cautiously hailed by other experts Thursday.

The team used a so-called “base editor”—an adaptation of the CRISPR-Cas9 DNA snipping tool—to correct a single, mutated “letter” among about three billion in the intricate coding of the human genome.

The targeted mutation can cause humans to be born with beta-Thalassaemia, a potentially fatal .

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This report on the NAD booster nicotinamide mononucleotide (NMN) will definetly be of interest to Lifeboat members.

NAD is the fountain of youth in mice and is boosted by NMN. This report includes highlights of Aug 2017 interview with Dr. David Sinclair, the researcher who discovered that the anti-aging molecule NAD has rejuvenating effects on mice.


Summary: NMN as a NAD-boosting anti-aging drug. Highlights of the August 2017 interview with David Sinclair, the scientist who discovered that the fountain of youth molecule NAD has remarkable rejuvenating effects on mice. The career of David Sinclair follows a link between sirtuins, resveratrol, NAD-boosting anti-aging compound nicotinamide mononucleotide (NMN), and calorie restriction.

Professor David A. Sinclair, Ph.D. has discovered what may be the fountain of youth. The Australian geneticist with the UNSW School of Medical Sciences and Harvard Medical School reported that by boosting NAD, a naturally-occurring compound found in our bodies, he was able to reverse DNA damage and turn elderly mice into energetic young ones.

So far, the only intervention that is known to increase lifespan in multiple species is caloric restriction (CR). Caloric restriction is known to increase lifespan in the majority of mouse strains tested[1]. The effects of CR have even been shown to influence how primates age and reduce the incidence of diabetes, cancer, cardiovascular disease, and brain atrophy[2].

Science has known about the effects of CR since the 1930s, when rat experiments first showed researchers this phenomenon[3]. However, despite the various health benefits of CR, how it delays aging has remained a mystery. A new study suggests that epigenetic drift may be the answer.

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We are very pleased to announce that Dr. Robert Shmookler Reis has joined the LEAF scientific advisory board. He studied at Harvard University (B.A.) and Sussex University (D.Phil.). He joined the University of Arkansas for Medical Sciences in 1980, where he holds the Udupa Chair of Gerontologic Research; he also serves as Affiliate Professor of Pathology at the Univ. of Washington in Seattle WA.

Dr. Robert Shmookler Reis is an expert in genetics whose work focuses on the molecular genetics of longevity and age-associated diseases and his team holds the world record for life extension in C. elegans (roundworms) making them live ten times their normal lifespan.

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THE numbers are stark. Cancer claimed the lives of 8.8m people in 2015; only heart disease caused more deaths. Around 40% of Americans will be told they have cancer during their lifetimes. It is now a bigger killer of Africans than malaria. But the statistics do not begin to capture the fear inspired by cancer’s silent and implacable cellular mutiny. Only Alzheimer’s exerts a similar grip on the imagination.

Confronted with this sort of enemy, people understandably focus on the potential for scientific breakthroughs that will deliver a cure. Their hope is not misplaced. Cancer has become more and more survivable over recent decades owing to a host of advances, from genetic sequencing to targeted therapies. The five-year survival rate for leukemia in America has almost doubled, from 34% in the mid-1970s to 63% in 2006-12. America is home to about 15.5m cancer survivors, a number that will grow to 20m in the next ten years. Developing countries have made big gains, too: in parts of Central and South America, survival rates for prostate and breast cancer have jumped by as much as a fifth in only a decade.

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Michio Kaku and Gregory Scott discuss different aspects of genetic engineering in the video below. According to Kaku and Scott, parents will soon have different genetic engineering choices to make about their children. In addition, recent discoveries by Yue Shao have yielded a new classification of parentless synthetic human embryos.

With Yue Shao’s discovery, genetic engineers might be learning to grow synthetic human embryos from anonymous stem cells donated from IVF clinics. How far this genetic engineering technology goes remains to be seen.

Michio Kaku and Gregory Scott speak about the ethical concerns of genetic engineering in the Michio Kaku video below beginning at the 29-minute mark. However, Yue Shao’s statements to MIT about the accidental discovery of how to engineer synthetic human embryos out of stem cells raises more ethical concerns.

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