Paper referenced in the video:
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/
Continue reading “Epigenetic Age Reduction Within 8 Weeks: Real Effect Or Statistical Noise?” »
One of the scientists prodding and poking the Kelly brothers is Prof Christopher E Mason, the lead geneticist on the Twins Study. Mason’s lab at Cornell University is nothing if not ambitious. Its work centres on a “500-year plan for the survival of the human species on Earth, in space, and on other planets.”
As well as studying what happens to astronauts, it involves laying the genetic groundwork for humans to live among the stars. Mason envisions a future in which the human genome can be bioengineered to adapt to almost any environment, augmented with genes from other species that allow us to explore and settle the farthest corners of the Universe.
We probably at this point should make all animals immortal: 3.
The advance promises to unlock new insights into human biology and disease, aiding in the study of everything from the developing immune system to tissue regeneration to skin cancer.
“Studying biodiversity is not just about exploring the biology of a bunch of interesting organisms, but ultimately for a better understanding of human biology,” developmental biologist and lead study author Hiroshi Kiyonari said via email.
Continue reading “Scientists produce first genetically engineered marsupials” »
The findings, published in Nature Communications, could have important implications for human health: minis have been found at every type of synapse studied so far, and defects in miniature neurotransmission have been linked to range of neurodevelopmental disorders in children. Figuring out how a reduction in miniature neurotransmission changes the structure of synapses, and how that in turn affects behavior, could help to better understand neurodegenerative disorders and other brain conditions.
Summary: Study reveals how miniature release events help to keep neurons intact and preserve motor neuron function in aging insects.
Source: EPFL
Continue reading “Brain ‘Noise’ Keeps Nerve Connections Young” »
Replacing Aging — Dr. Jean M. Hebert, Ph.D. Albert Einstein College of Medicine.
Dr. Jean M. Hebert, Ph.D. (https://einsteinmed.org/faculty/9069/jean-hebert/) is Professor in the Department of Genetics and in the Dominick P. Purpura Department of Neuroscience, at Albert Einstein College of Medicine.
To date, there are no effective antidotes against most virus infections. An interdisciplinary research team at the Technical University of Munich (TUM) has now developed a new approach: they engulf and neutralize viruses with nano-capsules tailored from genetic material using the DNA origami method. The strategy has already been tested against hepatitis and adeno-associated viruses in cell cultures. It may also prove successful against corona viruses.
“Our studies in mice revealed how genes co-operate to cause cancer in different organs. We identified main players, the order in which they occur during tumor progression, and the molecular processes how they turn normal cells into threatening cancers. Such processes are potential targets for new treatments”.
Why do alterations of certain genes cause cancer only in specific organs of the human body? Scientists at the German Cancer Consortium (DKTK), the Technical University of Munich (TUM), and the University Medical Center Göttingen have now demonstrated that cells originating from different organs are differentially susceptible to activating mutations in cancer drivers: The same mutation in precursor cells of the pancreas or the bile duct leads to fundamental different outcomes. The team discovered for the first time that tissue specific genetic interactions are responsible for the differential susceptibility of the biliary and the pancreatic epithelium towards transformation by oncogenes. The new findings could guide more precise therapeutic decision making in the future.
There have been no major improvements in the treatment of pancreatic and biliary tract cancer in the last decades and no effective targeted therapies are available to date. “The situation for patients with pancreatic and extrahepatic bile duct cancer is still very depressing with approximately only 10% of patients surviving five years,” says Dieter Saur, DKTK Professor for Translational Cancer Research at TUM’s university hospital Klinikum rechts der Isar, DKTK partner site Munich.
Continue reading “Why identical mutations cause different types of cancer” »
Encouraging Mid Trial data update! Great to know Dr. Katcher is applying for IRB approval for their human clinical trial for E5.
In this video we provide an update on Dr. Katcher’s experiment where he is treating rats with E5 (formerly called Elixer) on a regular schedule to see how long they will live for. Dr Katcher’s team have kindly provided some intermediate updates that we share in the video.
0:00 — 00:50 Introduction.
00:51 — 04:02 Project Background/Overview.
04:03 — Project Update.
NYU Abu Dhabi (NYUAD) researchers have uncovered a code that sets the genome of the liver to account for the remarkable ability for this organ to regenerate. This finding offers new insight into how the specific genes that promote regeneration can be activated when part of the liver is removed. These findings have the potential to inform the development of a new form of regenerative medicine that could help non-regenerative organs regrow in mice and humans.
While other animals can regenerate most organs, humans, mice, and other mammals can only regenerate their liver in response to an injury or when a piece is removed. NYUAD researchers hypothesized that the genes that drive regeneration in the liver would be controlled by a specific code that allows them to be activated in response to injury or resection. They home in on the epigenome, which is the modifications on the DNA that alter the gene expression, as opposed to changing the genetic code itself.
Using a mouse liver model, the team of NYUAD researchers, led by Professor of Biology Kirsten Sadler Edepli, identified the elements of the epigenetic code present in quiescent liver cells—cells that are currently not replicating but have the ability to proliferate under the right conditions—that activate specific genes to regenerate. Genes involved in liver cell proliferation are silenced in livers that are not regenerating, but the surprising finding was that they reside in parts of the genome where most genes are active. The researchers found that these pro-regenerative genes were marked with a specific modification—H3K27me3. During regeneration, H3K27me3 is depleted from these genes, enabling their dynamic expression and driving proliferation.
New research from the RIKEN Center for Brain Science (CBS) in Japan shows that a deficit in histone methylation could lead to the development of autism spectrum disorders (ASD). A human variant of the SUV39H2 gene led researchers to examine its absence in mice. Published in Molecular Psychiatry, the study found that when absent, adult mice exhibited cognitive inflexibility similar to what occurs in autism, and embryonic mice showed misregulated expression of genes related to brain development. These findings represent the first direct link between the SUV39H2 gene and ASD.
Genes are turned on and off throughout our development. But genetic variation means that what is turned off in some people remains turned on in others. This is why, for example, some adults can digest dairy products and others are lactose intolerant; the gene for making the enzyme lactase is turned off when some people become adults, but not others. One way that genes can be turned on and off is through a process called histone methylation in which special enzymes transfer methyl groups to histone proteins that are wrapped around DNA.
Variations in genes related to methylation during brain development can lead to serious problems. One such variation occurs in a rare disorder called Kleefstra Syndrome, in which a mutation prevents methylation of H3K9—a specific location on histone H3. Because Kleefstra Syndrome resembles autism in some ways, RIKEN CBS researchers led by Takeo Yoshikawa looked for autism-specific variations in genes that can modify H3K9. Among nine such genes, they found one variant in an H3K9 methyltransferase gene— SUV39H2 —that was present in autism, and the mutated SUV39H2 prevented methylation when tested in the lab. Similar loss-of-function results were found for the mouse version of the variant.
