Lifeboat Foundation

One can only hope.

A former Google engineer has just predicted that humans will achieve immortality in eight years, something more than likely considering that 86% of his 147 predictions have been correct.

Ray Kurzweil visited the YouTube channel Adagio, in a discussion on the expansion of genetics, nanotechnology and robotics, which he believes will lead to age-reversing ‘nanobots’.

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The actor Bruce Willis was diagnosed with aphasia in April 2022—updated in February 2023 to frontotemporal dementia (FTD). Now, a major advancement is helping develop new treatments for some people with motor neuron diseases, including FTD and ALS, possibly including a nasal spray that could help prevent the genetic disease.

A recently patented genome editing tool called PASTE holds genuine promise for expanding the universe of treatable genetic diseases. The approach combines elements of CRISPR and prime editing with a pair of enzymes designed to enable the integration of large segments of DNA without incurring double-stranded DNA breaks.

U.S. Patent No. 11,572,556, assigned to MIT, covers systems, methods, and compositions for programmable addition via site-specific targeting elements (PASTE). The patent describes site-specific integration of a nucleic acid into a genome, using a CRISPR–Cas9 nickase fused to a reverse transcriptase (RT) and a serine integrase. These enzymes target specific genome sequences known as attachment sites, binding to them before integrating their DNA payload.

PASTE can insert DNA fragments as large as 50,000 base pairs, which puts it on a different plane compared to other genome editing tools such as prime editing.

A new CRISPR tool corrected a genetic mutation that causes vision loss, in an experiment in mice — and its creators at the Wuhan University of Science and Technology (WUST) in China think it could be a safe way to treat countless other genetic diseases in people.

The challenge: Vision starts with light entering the eye and traveling to the retina. There, light-sensitive cells, called photoreceptors, convert light into electrical signals that are sent to the brain.

Retinitis pigmentosa is a rare — and, currently, incurable — genetic disease that can be caused by mutations in more than 100 different genes. These mutations destroy the cells of the retina, leading to vision loss, and for most people, there’s no way to stop the disease or reverse its damage (the exception is a gene therapy approved to treat mutations in the RPE65 gene).

Scientists at St. Jude Children’s Research Hospital and Rockefeller University have combined their expertise to gain a better understanding of the cystic fibrosis transmembrane conductance regulator (CFTR). Mutations in CFTR cause cystic fibrosis, a fatal disease with no cure.

Current therapies using a drug called a potentiator can enhance CFTR functions in some patients; but how the potentiators work is not well understood. The new findings reveal how CFTR functions mechanistically and how disease mutations and potentiators affect those functions. With this information, researchers may be able to design more effective therapies for cystic fibrosis. The study was published today in Nature.

Cystic fibrosis is a genetic disorder that causes people to produce mucus that is too thick and sticky. This can block airways and lead to lung damage as well as cause problems with digestion. The disease affects about 35,000 people in the United States. CFTR is an anion channel, a passageway that maintains the right balance of salts and fluid across epithelial and other membranes. Mutations in CFTR are what cause cystic fibrosis, but these mutations can affect CFTR function differently. Therefore, some drugs used to treat the disease can only partially restore function of specific mutant forms of CFTR.

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The researchers add that these data demonstrate that CRISPRa is generally applicable across chromatin states and cell types, and highlights the factors that impact the degree of gene activation and how easy it is to reproduce the effects. Understanding these factors is important in the design and analysis of CRISPRa screens, which are used to look for genes involved in genetic diseases, the team points out.

Further study is required to continue to add to these rules and to see whether different CRISPRa or CRISPR interference techniques behave in a similar way.

“Our research has established a system for reporting the effectiveness of CRISPR activation in stem cells, allowing us to gain a better understanding of how CRISPRa works in multiple cell states,” says Qianxin Wu, PhD, first author from Wellcome Sanger. “We also showed that CRISPR gene activation is powerful enough to induce stem cells to differentiate into other cell states. This suggests that CRISPRa screens can be used to search for genes involved in cellular processes or to generate more accurate models of cell types in the body, aiding research into genetic diseases and regenerative medicine.”

Induced pluripotent stem cells offer great therapeutic potential and are a valuable tool for understanding how different diseases develop. New research shows that such stem cell lines should be regularly screened for genetic mutations to ensure the accuracy of the disease models.

In the past 10 years, scientists have learned to create induced pluripotent stem cells (iPSC) from ordinary cells by genetic reprogramming. These cells are widely used to study diseases, as they can be differentiated to almost any cell type of the body, and they can be generated from any individual. However, a key remaining methodological challenge is that the differentiation process is subject to major technical variation for mostly unknown reasons.

HiLIFE Tenure Track Professor Helena Kilpinen and her group at the University of Helsinki use stem cells for studying the biological mechanisms of neurodevelopmental and other brain-related diseases.

Michael Levin is a biologist at Tufts University working on novel ways to understand and control complex pattern formation in biological systems.

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