The result is optogenetics, a mind-controlling technique that’s become one of neuroscience’s most popular tools. Here, scientists use genetic engineering to put different types of algae proteins into the brains of mice. They can then activate a neuron with an implanted fiber optic cable by pulsing certain wavelengths of light. These enhanced brain cells react as they would naturally, generating an electrical signal that’s passed down and interpreted by the mouse’s brain.
Sound familiar?
If an algae protein can artificially allow neurons in the brain to translate light into electrical information, why can’t it do the same for damaged eyes?
A summary of the sequel trial for a cocktail of drugs that originally turned back epigenetic clocks by 2.5 years. I do wonder what effect plasma filtering has on the thymus if any.
In this video we review the TRIIM study and look at the trial document for TRIIM-X, the extension study that Dr. Fahy is now conducting.
Timing — If you are familiar with the TRIIM Study please use the time links below to jump to TRIIM-X 0:12 : TRIIM Paper Review. 7:11 : TRIIM-X Trial Review. 08:59 : TRIIM vs TRIIM-X
Papers referred to in this video. Reversal of epigenetic aging and immunosenescent trends in humans Sept 2019 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826138/
Thymus Regeneration, Immunorestoration, and Insulin Mitigation Extension Trial (TRIIM-X) https://clinicaltrials.gov/ct2/show/NCT04375657
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Mount Sinai researchers have developed a therapeutic agent that shows high effectiveness in vitro at disrupting a biological pathway that helps cancer survive, according to a paper published in Cancer Discovery, a journal of the American Association for Cancer Research, in July.
The therapy is an engineered molecule, named MS21, that causes the degradation of AKT, an enzyme that is overly active in many cancers. This study laid out evidence that pharmacological degradation of AKT is a viable treatment for cancers with mutations in certain genes.
AKT is a cancer gene that encodes an enzyme that is frequently abnormally activated in cancer cells to stimulate tumor growth. Degradation of AKT reverses these processes and inhibits tumor growth.
Timecodes: 0:00-Introduction. 0:17-Amygdala role in fear regulation. 0:45-Difficulties in exploring prey-predator interaction. 1:02-Lego robot to simulate a predator. Robogator (LEGO Mindstorms robot) 1:53-Fear response before the amygdala inactivation. 2:33-Fear response aftert the amygdala inactivation. 3:59-Amygdala is one of the key regions of the fear regulation. 4:50 — Human-based experiments on the electrical stimulation of amygdala. 6:01-Future prospects. Optogenetics. 6:34-Share your ideas and emotions in the comments.
In this video I review a scientific neuroscience publication :“Amygdala regulates risk of predation in rats foraging in a dynamic fear environment” from University of Washington and Korea University, Seoul. The scientific paper addresses the mechanism of fear regulation in rats. Neuroscientists inactivated neurons of the brain region regulating fear — amygdala. In order to inactivate amygdala neurons neurobiologists applied GABAA receptor agonist muscimol. In this way neuroscientists made the rat fearless. Neurobiologists simulated fear enviroment by using lego robot — Robogator (LEGO Mindstorms robot) programmed to surge toward the animal as it emerges from the nesting area in search of food.
Neuroscientists also increased the activity of amygdala neurons by applying GABAA receptor antagonist bicuculline methiodide. In this way neuroscience researchers increased the fear response of the laboratory rodent.
Similar role of amygdala in fear regulation was demonstrated for humans. For instance, in 2007 neuro researchers from Universite de Provence from France in their paper :” Emotion induction after direct intracerebral stimulations of human amygdala ” electrically stimulated amygdala and could induce negative emotions that were either verbally self-reported by a participant or measured by physiological markers such as skin conductance.
The human body is essentially made up of trillions of living cells. It ages as its cells age, which happens when those cells eventually stop replicating and dividing. Scientists have long known that genes influence how cells age and how long humans live, but how that works exactly remains unclear. Findings from a new study led by researchers at Washington State University have solved a small piece of that puzzle, bringing scientists one step closer to solving the mystery of aging.
A research team headed by Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of cells. The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).
The telomerase gene controls the activity of the telomerase enzyme, which helps produce telomeres, the caps at the end of each strand of DNA that protect the chromosomes within our cells. In normal cells, the length of telomeres gets a little bit shorter every time cells duplicate their DNA before they divide. When telomeres get too short, cells can no longer reproduce, causing them to age and die. However, in certain cell types—including reproductive cells and cancer cells —the activity of the telomerase gene ensures that telomeres are reset to the same length when DNA is copied. This is essentially what restarts the aging clock in new offspring but is also the reason why cancer cells can continue to multiply and form tumors.
Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.
In a study published today in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain — ‘scaffolding’ around nerve cells—lead to loss of memory with aging, but that it is possible to reverse these using genetic treatments.
Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity—the ability of the brain to learn and adapt—and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimized. Then, plasticity is partially turned off, making the brain more efficient but less plastic.
In March 2017, Read and his Penn State colleague David Kennedy published a paper in the Proceedings of the Royal Society B in which they outlined several strategies that vaccine developers could use to ensure that future vaccines don’t get punked by evolutionary forces. One overarching recommendation is that vaccines should induce immune responses against multiple targets. A number of successful, seemingly evolution-proof vaccines already work this way: After people get inoculated with a tetanus shot, for example, their blood contains 100 types of unique antibodies, all of which fight the bacteria in different ways. In such a situation, it becomes much harder for a pathogen to accumulate all the changes needed to survive. It also helps if vaccines target all the known subpopulations of a particular pathogen, not just the most common or dangerous ones. Richard Malley and other researchers at Boston Children’s Hospital are, for instance, trying to develop a universal pneumococcal vaccine that is not serotype-specific.
Vaccines should also bar pathogens from replicating and transmitting inside inoculated hosts. One of the reasons that vaccine resistance is less of a problem than antibiotic resistance, Read and Kennedy posit, is that antibiotics tend to be given after an infection has already taken hold — when the pathogen population inside the host is already large and genetically diverse and might include mutants that can resist the drug’s effects. Most vaccines, on the other hand, are administered before infection and limit replication, which minimizes evolutionary opportunities.
But the most crucial need right now is for vaccine scientists to recognize the relevance of evolutionary biology to their field. Last month, when more than 1000 vaccine scientists gathered in Washington, D.C., at the World Vaccine Congress, the issue of vaccine-induced evolution was not the focus of any scientific sessions. Part of the problem, Read says, is that researchers are afraid: They’re nervous to talk about and call attention to potential evolutionary effects because they fear that doing so might fuel more fear and distrust of vaccines by the public — even though the goal is, of course, to ensure long-term vaccine success. Still, he and Kennedy feel researchers are starting to recognize the need to include evolution in the conversation. “I think the scientific community is becoming increasingly aware that vaccine resistance is a real risk,” Kennedy said.
Nature always finds a way…so they say! But it looks like it may actually be true in the case of our global plastic waste dilemma. Genetic mutations have been discovered in specific natural bacteria that enable them to break the polymer chains of certain plastics. Where have we found these bacteria? Well…in plastic recycling dumps of course. So, gloves and masks on everyone. We’re going in!
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To quickly express learning and memory genes, brain cells snap both strands of DNA in many more places and cell types than previously realized, a new study shows.
The urgency to remember a dangerous experience requires the brain to make a series of potentially dangerous moves: Neurons and other brain cells snap open their DNA in numerous locations — more than previously realized, according to a new study — to provide quick access to genetic instructions for the mechanisms of memory storage.
The extent of these DNA double-strand breaks (DSBs) in multiple key brain regions is surprising and concerning, says study senior author Li-Huei Tsai, Picower Professor of Neuroscience at MIT and director of The Picower Institute for Learning and Memory, because while the breaks are routinely repaired, that process may become more flawed and fragile with age. Tsai’s lab has shown that lingering DSBs are associated with neurodegeneration and cognitive decline and that repair mechanisms can falter.
Potential reversal of epigenetic age using a diet and lifestyle. intervention: a pilot randomized clinical trial. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8064200/
