Lifeboat Foundation

A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.

In a study, published in the journal eLife on September 29, 2020, the researchers identified a factor that acts like a molecular switch in the skin of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goosebumps, an ability that is lost in adult human scars.

“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Ryan Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”

When the brain forms a memory of a new experience, neurons called engram cells encode the details of the memory and are later reactivated whenever we recall it. A new MIT study reveals that this process is controlled by large-scale remodeling of cells’ chromatin.

This remodeling, which allows specific genes involved in storing memories to become more active, takes place in multiple stages spread out over several days. Changes to the density and arrangement of chromatin, a highly compressed structure consisting of DNA and proteins called histones, can control how active specific genes are within a given cell.

“This paper is the first to really reveal this very mysterious process of how different waves of genes become activated, and what is the epigenetic mechanism underlying these different waves of gene expression,” says Li-Huei Tsai, the director of MIT’s Picower Institute for Learning and Memory and the senior author of the study.

Summary: The ability to foster and form secure interpersonal attachments can mitigate some of the genetic risks associated with PTSD.

Source: Yale

Researchers at Yale and elsewhere previously identified a host of genetic risk factors that help explain why some veterans are especially susceptible to the debilitating symptoms of post-traumatic stress disorder (PTSD).

An experimental new vaccine claims to be able to change human DNA and could be deployed against COVID-19 by 2021 through a biochip implant.

The most significant scientific discovery since gravity has been hiding in plain sight for nearly a decade and its destructive potential to humanity is so enormous that the biggest war machine on the planet immediately deployed its vast resources to possess and control it, financing its research and development through agencies like the National Institutes of Health (NIH), the Defense Advanced Research Projects Agency (DARPA) and HHS’ BARDA.

The revolutionary breakthrough came to a Canadian scientist named Derek Rossi in 2010 purely by accident. The now-retired Harvard professor claimed in an interview with the National Post that he found a way to “reprogram” the molecules that carry the genetic instructions for cell development in the human body, not to mention all biological lifeforms.

Continue reading “A DARPA-Funded Implantable Biochip to Detect COVID-19 Could Hit Markets by 2021” »

In the coming 2020s, the world of medical science will make some significant breakthroughs. Through brain implants, we will have the capability to restore lost memories.

~ The 2020s will provide us with the computer power to make the first complete human brain simulation. Exponential growth in computation and data will make it possible to form accurate models of every part of the human brain and its 100 billion neurons.

~ The prototype of the human heart was 3D printed in 2019. By the mid- 2020s, customized 3D- printing of major human body organs will become possible. In the coming decades, more and more of the 78 organs in the human body will become printable.

Continue reading “The Road to Human 2.0” »

A new, rare genetic form of dementia has been discovered by a team of Penn Medicine researchers. This discovery also sheds light on a new pathway that leads to protein build up in the brain—which causes this newly discovered disease, as well as related neurodegenerative diseases like Alzheimer’s Disease—that could be targeted for new therapies. The study was published today in Science.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a buildup of proteins, called tau proteins, in certain parts of the brain. Following an examination of human brain tissue samples from a deceased donor with an unknown neurodegenerative disease, researchers discovered a novel mutation in the Valosin-containing protein (VCP) gene in the brain, a buildup of tau proteins in areas that were degenerating, and neurons with empty holes in them, called vacuoles. The team named the newly discovered disease Vacuolar Tauopathy (VT)—a neurodegenerative disease now characterized by the accumulation of neuronal vacuoles and tau protein aggregates.

“Within a cell, you have proteins coming together, and you need a process to also be able to pull them apart, because otherwise everything kind of gets gummed up and doesn’t work. VCP is often involved in those cases where it finds proteins in an aggregate and pulls them apart,” Edward Lee, MD, Ph.D., an assistant professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. “We think that the mutation impairs the proteins’ normal ability to break aggregates apart.”

Researchers at Rockefeller University have just released findings from a new study, done in mice, which identifies a gene that is critical for short-term memory but functions in a part of the brain not traditionally associated with memory. Classical models for short-term memory typically assume that all neuronal activity is contained within the prefrontal cortex (PFC), yet, data from this new study suggests that a G-protein coupled receptor in the thalamus may play a large role. Data from the study was published recently in Cell through an article titled “A Thalamic Orphan Receptor Drives Variability in Short Term Memory.”

Interestingly, in order to discover new genes and brain circuits that are important for short-term memory, the researchers turned to studying genetically diverse mice, rather than inbred mice commonly used in research.

“We needed a population that is diverse enough to be able to answer the question of what genetic differences might account for variation in short-term memory,” explained co-senior study investigator Praveen Sethupathy, PhD, an associate professor of biomedical sciences in Cornell’s College of Veterinary Medicine and director of the Cornell Center for Vertebrate Genomics.

Genes inherited from Neanderthal ancestors may be involved in some cases of severe Covid-19 disease, researchers in Germany reported Wednesday.

A team of experts on Neanderthal genetics examined a strand of DNA that has been associated with some of the more serious cases of Covid-19 and compared it to sequences known to have been passed down to living Europeans and Asians from Neanderthal ancestors.

The DNA strand is found on chromosome 3, and a team of researchers in Europe has linked certain variations in this sequence with the risk of being more severely ill with Covid-19.

A combined analysis using people of Japanese, Chinese, and European ancestry identified five new genes associated with the non-familial, sporadic form of amyotrophic lateral sclerosis (ALS).

These findings further an understanding of the genetic basis of sporadic ALS, and may support the development of new therapies.