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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 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.

These molecules are called ‘messenger ribonucleic acid’ or mRNA and the newfound ability to rewrite those instructions to produce any kind of cell within a biological organism has radically changed the course of Western medicine and science, even if no one has really noticed yet. As Rossi, himself, puts it: “The real important discovery here was you could now use mRNA, and if you got it into the cells, then you could get the mRNA to express any protein in the cells, and this was the big thing.”

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.

…As we enter into the next few decades, we will have the technologies that grant us the possibility of immortality, albeit one that is highly subjective.

With our ability to 3D print new body organs, our ability to use nanotechnology in fighting death at cellular levels, our ability to use CRISPR or other gene-editing technology to rewrite our definition of humans and even our ability to capture and extend our consciousness beyond the confines of the biological weakness of our human bodies — immortality may be within reach of our fingers as depicted in the painting of Michelangelo.

The race to human 2.0 will be run broadly in two spectrums — the evolution of our body and the evolution of our minds.

Excerpt from my book — 2020s & The Future Beyond.

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 (AD) is a neurodegenerative disease characterized by a buildup of proteins, called , 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.

Some people are at higher risk of developing obesity because they possess genetic variants that affect how the brain processes sensory information and regulates feeding and behavior. The findings from scientists at the University of Copenhagen support a growing body of evidence that obesity is a disease whose roots are in the brain.

Over the past decade, scientists have identified hundreds of different genetic variants that increase a person’s risk of developing obesity. But a lot of work remains to understand how these variants translate into obesity. Now scientists at the University of Copenhagen have identified populations of cells in the that play a role in the development of the disease—and they are all in the brain.

“Our results provide evidence that outside the traditional organs investigated in obesity research, such as , play a key role in human obesity,” says Associate Professor Tune H Pers from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR), at the University of Copenhagen, who published his team’s findings in the internationally-recognized journal eLife.

Two active genetics strategies help address concerns about gene-drive releases into the wild.

In the past decade, researchers have engineered an array of new tools that control the balance of genetic inheritance. Based on CRISPR technology, such gene drives are poised to move from the laboratory into the wild where they are being engineered to suppress devastating diseases such as mosquito-borne malaria, dengue, Zika, chikungunya, yellow fever and West Nile. Gene drives carry the power to immunize mosquitoes against malarial parasites, or act as genetic insecticides that reduce mosquito populations.

Although the newest gene drives have been proven to spread efficiently as designed in laboratory settings, concerns have been raised regarding the safety of releasing such systems into wild populations. Questions have emerged about the predictability and controllability of gene drives and whether, once let loose, they can be recalled in the field if they spread beyond their intended application region.