Disrupting a gene responsible for pigments allowed experts in Kobe, Japan to create albino opossum offspring.
Category: genetics – Page 364
Researchers identify a cellular defect common to familial and sporadic forms of ALS
This study builds on an earlier paper by the Rothstein lab that looked at the most common genetic cause of ALS, a mutation in the C9orf72 gene (also referred to as the “C9 mutation”). There, they showed that the C9 mutation produced defects in a structure called the nuclear pore that is responsible for moving proteins and other molecules in and out of the nucleus of cells.
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal degenerative disease affecting the nerve cells in the brain and spinal cord responsible for controlling voluntary muscle movement. “Sporadic” or non-inherited ALS, accounts for roughly 90% percent of cases, and 10% of cases are due to known genetic mutations. By studying lab-grown neurons derived from skin or blood cells from 10 normal controls, eight with an ALS causing mutation, and 17 with non-inherited ALS, researchers have found a possible starting point for the dysfunction that causes the disease. The study, which was published in Science Translational Medicine, was funded in part by the National Institute for Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
Using a library of ALS patient-derived cells, the research team led by Jeffrey Rothstein, M.D., Ph.D., at Johns Hopkins University School of Medicine, Baltimore, developed induced pluripotent stem cell (iPSC)-derived neurons from the patients’ cultured cells to discover a common defect regardless of whether the cell came from persons with inherited or non-inherited ALS. They report that in ALS nerve cells, there is an accumulation of a protein called CHMP7 in the nucleus of cultured nerve cells as well as in ALS samples from the brain region that controls movement. Treatments that decrease the amount of CHMP7 in the cultured cells prevented a series of abnormalities that are characteristic of ALS.
“There is considerable interest in identifying new therapeutic targets for ALS, particularly for the sporadic form of the disorder,” said Amelie Gubitz, Ph.D., program director, NINDS. “Gene-targeting strategies like the one shown here now allow us to move from biological discovery straight to therapy development.”
How An Altered Strand Of DNA Can Cause Malaria-Spreading Mosquitoes To Self-Destruct
Despite years of efforts, malaria remains a major health problem. The mosquito-borne parasitic disease sickens more than 200 million people every year and kills more than 400000, many of whom are children.
For the first time, scientists have shown that a new kind of genetic engineering can crash populations of malaria-spreading mosquitoes.
In the landmark study, published Wednesday in the journal Nature Communications, researchers placed the genetically modified mosquitoes in a special laboratory that simulated the conditions in sub-Saharan Africa, where they spread the deadly disease.
The male mosquitoes were engineered with a sequence of DNA known as a “gene drive” that can rapidly transmit a deleterious mutation that essentially wipes out populations of the insects.
Genetic requirements for cell division in a genomically minimal cell
A reverse genetics approach determined that seven genes are required together for normal cell division in a genomically minimal cell; these include two known cell division genes, ftsZ and sepF, a hydrolase of unknown substrate, and four genes that encode membrane-associated proteins of unknown function.
Quantifying Biological Age: Blood Test #3 in 2021
Links to biological age calculators:
Levine’s PhenoAge calculator is embedded as an Excel file:
Papers referenced in the video:
A new aging measure captures morbidity and mortality risk across diverse subpopulations from NHANES IV: A cohort study.
https://pubmed.ncbi.nlm.nih.gov/30596641/
Underlying features of epigenetic aging clocks in vivo and in vitro.
https://onlinelibrary.wiley.com/doi/full/10.1111/acel.
Population Specific Biomarkers of Human Aging: A Big Data Study Using South Korean, Canadian, and Eastern European Patient Populations.
TAME Q&A: Lessons for Progress on Aging | Nir Barzilai, Albert Einstein School of Medicine
More TAME! The first part of this has a lot of result data.
Foresight Biotech & Health Extension Meeting sponsored by 100 Plus Capital.
2021 program & apply to join: https://foresight.org/biotech-health-extension-program/
Nir Barzilai, Albert Einstein School of Medicine.
TAME Q&A: Lessons for Progress on Aging.
About Nir Barzilai:
Nir Barzilai, MD, is a Professor in the Department of Endocrinology Medicine and the Department of Genetics at the Albert Einstein College of Medicine. He is also the Ingeborg and Ira Leon Rennert Chair of Aging Research at the Albert Einstein College of Medicine. Dr. Barzilai is the founding director of the Institute for Aging Research at Albert Einstein College of Medicine and the Director of the Nathan Shock Center for Excellence in the Basic Biology of Aging, funded by the National Institutes of Health (NIH); the center is coordinating 80 investigators and six program projects on the biology of aging. He is also the director of the Glenn Center of Excellence in the Biology of Human Aging. He is a chaired professor of medicine and of genetics and a member of the Diabetes Research Center and the divisions of endocrinology and geriatrics. Dr. Barzilai’s interests focus on several basic mechanisms in the biology of aging, including the biological effects of nutrients on extending life and the genetic determinants of life span. His team discovered many longevity gene in humans, and they further characterized the phenotype and genotype of humans with exceptional longevity through NIH awards. He also has an NIH Merit award investigating the metabolic decline that accompanies aging and its impact on longevity. Dr. Barzilai has published more than 270 peer-reviewed papers, reviews and chapters in textbooks. Dr. Barzilai serves on several editorial boards and advisory boards of pharmaceutical and start-up companies, and is a reviewer for numerous journals. A Beeson Fellow for Aging Research, Dr. Barzilai has received many other prestigious awards, including the Senior Ellison Foundation Award, the 2010 Irving S. Wright Award of Distinction in Aging Research, the NIA–Nathan Shock Award and a merit award from the NIA for his contributions in elucidating metabolic and genetic mechanisms of aging and was the 2018 recipient of the IPSEN Longevity award. He is leading the TAME (Targeting/Taming Aging with Metformin) Trial, a multi-center study to prove the concept that multi morbidities of aging can be delayed in humans and change the FDA indications to allow for next generation interventions. He is a founder of CohBar Inc. (now public company) and Medical Advisor for Life Biosciences. He is on the board of AFAR and a founding member of the Academy for Lifespan and Healthspan. He has been featured in major papers, TV programs, and documentaries (TEDx and TEDMED) and has been consulting or presented the promise for targeting aging at The Singapore Prime Minister Office, several International Banks, The Vatican, Pepsico, Milkin Institute, The Economist and Wired Magazine. His book, Age Later: Health Span, Life Span, and the New Science of Longevity, was published by St. Martin’s Press in June of 2020.
Zoom Transcription: https://otter.ai/u/0bz5o2crLQncfxlUkctY6NVzcCg.
How Gene Therapy and Algae Proteins Partially Restored a Blind Man’s Sight
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?
TRIIM-X 2nd Phase Clinical Trial For Reversing Human Aging | Study Review
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)
New Gene Therapy Developed That Could Be Effective Against Many Types of Cancer
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.
Scientists made this rat fearless
Neuroscientists removed fear from rats by inactivating amygdala — brain region mediating fear.
#Neuroscience #Brain #YuriNeuro #Neurobiology #Amygdala.
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.