O,.o.
Ever wanted to get rid of a memory that holds you back or torments you? Well, you might soon be able to.
In an experiment out of the films Total Recall and Eternal Sunshine Of The Spotless Mind, painful experiences have been erased from the brain.
It is down to Tet1, a gene that overwrites old memories with new ones.
Summary: A patient who suffered brain injury can temporarily walk, talk, and recognize family members thanks to the sleep medication Zolpidem.
Source: Radboud University
A patient who could not move and talk spontaneously for eight years started to do so again after being administered a sleeping pill. The spectacular but temporary effect was visualized with brain scans, giving researchers from Radboud university medical center and Amsterdam UMC a better understanding of this disorder’s underlying neurophysiological processes. The article has been published in Cortex.
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).
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.
#Future #Humanity #Transhumanism
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.
Fecal transplants could one day be used as a therapy to restore cognitive function in the elderly—according to new research from the University of East Anglia, the University of Florence and the Quadram Institute.
A new study published today shows how fecal transplants from older to younger mice altered their gut microbiome, which in turn impacted their spatial learning and memory.
The research team hope that reversing the procedure could one day see fecal transplantation used to combat cognitive decline among the elderly.
Researchers have identified a bio-chemical circuit that supports neuron-microglia communication. When neurons are active, they release ATP. Microglia sense extracellular ATP and the compound draws the immune cell toward the neuron.circuit that supports neuron-microglia communication. When neurons are active, they release ATP. Microglia sense extracellular ATP and the compound draws the immune cell toward the neuron.circuit that supports neuron-microglia communication. When neurons are active, they release ATP. Microglia sense extracellular ATP and the compound draws the immune cell toward the neuron.
Han from WrySci HX gives you a few different reasons why Neuralink is not quite as scary as you may think, especially if you’re not super familiar in the brain machine interface area. Share with a skeptic! More below ↓↓↓
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Stem cells are a promising experimental treatment for a variety of diseases. Now researchers at the University of Wisconsin-Madison have found that transplanting neurons grown from stem cells into the brains of mice with Parkinson’s disease repaired the damaged brain circuits, improving the animals’ motor skills.
In people afflicted with Parkinson’s, neurons that produce dopamine begin to break down and die. The disease gradually presents as tremors, involuntary movements, and trouble with walking, speaking and other actions. While it currently can’t be cured, studies are suggesting new ways to slow progression and reduce severity of symptoms through new drugs or repurposed old ones, deep brain stimulation or probiotic treatments.
But an emerging and potentially ground-breaking treatment involves stem cells. In several studies, researchers have used stem cells to grow new dopamine-producing neurons, and then transplant them into animals. And now the UW-Madison team’s work has shown that doing so can help restore brain circuits damaged by Parkinson’s.
