Lifeboat Foundation

Concretely: even with advanced technologies, it is impossible to predict someone’s behaviour based on their facial features. Peter Claes continues, Our results confirm that there is no genetic evidence for a link between someone’s face and that individual’s behaviour. Therefore, we explicitly dissociate ourselves from pseudoscientific claims to the contrary.

Claes said, To be able to analyse the MRI scans, we had to measure the brains shown on the scans. Our specific focus was on variations in the folded external surface of the brain – the typical ‘walnut shape’. We then went on to link the data from the image analyses to the available genetic information. This way, we identified 472 genomic locations that have an impact on the shape of our brain. 351 of these locations have never been reported before. To our surprise, we found that as many as 76 genomic locations predictive of the brain shape had previously already been found to be linked to the face shape. This makes the genetic link between face and brain shape a convincing one.

The team also found evidence that genetic signals that influence both brain and face shape are enriched in the regions of the genome that regulate gene activity during embryogenesis, either in facial progenitor cells or in the developing brain.

For the uninitiated, “Jurassic Park” and “Jurassic World” make up a five-movie franchise — with a sixth in the works — all based on Michael Crichton’s hit novel about how bad of an idea it was to open a place like Jurassic Park. Leveraging recent advances in genetic research to create entirely new creatures is certainly an enticing idea, though there’s a big difference between something potentially being feasible and actually being a good idea.

But it’s not all fun and games when you’re playing god and creating new dinosaurs. Hodak later added that de-extinction could be a valuable tool for increasing biodiversity, perhaps because we find ourselves in the midst of an era of mass extinction.

“Biodiversity (antifragility) is definitely valuable; conservation is important and makes sense,” Hodak tweeted minutes later. “But why do we stop there? Why don’t we more intentionally try to generate novel diversity?”

A patient with a genetic form of childhood blindness gained vision, which lasted more than a year, after receiving a single injection of an experimental RNA therapy into the eye.

The gene editing research was conducted at the Perelman School of Medicine in the University of Pennsylvania. Results of the case, detailed in a paper published April 1 in Nature Medicine, show that the treatment led to marked changes at the fovea, the most important point of human central vision.

In the international clinical trial, participants received an intraocular injection of an antisense oligonucleotide called sepofarsen. This short RNA molecule works by increasing normal CEP290 protein levels in the eye’s photoreceptors and improving retinal function under day vision conditions.

The team found that feeding mice a high fat diet disrupted the circuit, which led not only to weight gain but also to signs of anxiety and depression on standard behavioral tests.

When the researchers used genetic techniques to restore the normal functioning of nerve receptors in the circuit, this resulted in weight loss and eliminated the animals’ signs of anxiety and depression.

A recent study in mice has found that eating a high fat diet may disrupt a newly discovered neural circuit that affects both mood and appetite.

Continue reading “Faulty brain circuit helps explain obesity–depression link” »

This genetic connection caught many scientists off guard, and it remains “one of the most intriguing and poorly understood events in human history,” the researchers wrote in the new study.

To investigate the Y signal further, a team of scientists in Brazil and Spain dove into a large dataset containing the genetic data of 383 Indigenous people from different parts of South America. The team applied statistical methods to test whether any of the Native American populations had “excess” genetic similarity with a group they called the Australasians, or Indigenous peoples from Australia, Melanesia, New Guinea and the Andaman Islands in the Indian Ocean.

In other words, the team was assessing whether “a given Native American population shared significantly more genetic variants with Australasians than other Native Americans do,” Hünemeier and Araújo Castro e Silva said. South American groups that did have more genetic similarities with Australasians were interpreted by the new researchers as being descendants of the first Americans and Australasian ancestors, who coupled together at least 15000 years ago.

Today, we chronicle the progress of partial cellular reprogramming and discuss how this powerful treatment may be able to reprogram cells back into a youthful state, at least partially reversing epigenetic alterations, one of the proposed reasons we age.

For those of you new to the subject of epigenetic alterations you can learn more by clicking on the topic box below, for the more seasoned readers, feel free to skip ahead.

Gene editing has shown great promise as a non-heritable way to treat a wide range of conditions, including many genetic diseases and more recently, even COVID-19. But could a version of the CRISPR gene-editing tool also help deliver long-lasting pain relief without the risk of addiction associated with prescription opioid drugs?

In work recently published in the journal Science Translational Medicine, researchers demonstrated in mice that a modified version of the CRISPR system can be used to “turn off” a gene in critical neurons to block the transmission of pain signals [1]. While much more study is needed and the approach is still far from being tested in people, the findings suggest that this new CRISPR-based strategy could form the basis for a whole new way to manage chronic pain.

This novel approach to treating chronic pain occurred to Ana Moreno, the study’s first author, when she was a Ph.D. student in the NIH-supported lab of Prashant Mali, University of California, San Diego. Mali had been studying a wide range of novel gene-and cell-based therapeutics. While reading up on both, Moreno landed on a paper about a mutation in a gene that encodes a pain-enhancing protein in spinal neurons called NaV1.7.

“The axons of nerve cells function a bit like a railway system, where the cargo is essential components required for the cells to survive and function. In neurodegenerative diseases, this railway system can get damaged or blocked,” Tasneem Khatib, the study’s first author, explained in a statement. “We reckoned that replacing two molecules that we know work effectively together would help to repair this transport network more effectively than delivering either one alone, and that is exactly what we found.”

Most neurodegenerative diseases are caused by multiple genetic abnormalities, making them difficult to address with gene therapy targeted at single mutations. Astellas is working on a gene therapy that expresses two proteins, and a University of Cambridge team has shown that it holds promise in glau…

UC scientists and physicians hope to permanently cure patients of sickle cell disease by using CRISPR-Cas9 to replace a defective gene with the normal version.

In 2014, two years after her Nobel Prize-winning invention of CRISPR-Cas9 genome editing, Jennifer Doudna thought the technology was mature enough to tackle a cure for a devastating hereditary disorder, sickle cell disease, that afflicts millions of people around the world, most of them of African descent. Some 100000 Black people in the U.S. are afflicted with the disease.

Continue reading “FDA approves first test of CRISPR to correct genetic defect causing sickle cell disease” »