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Category: biotech/medical – Page 1,968

Harvard Professor Wants to Slow Down & Reverse Aging: David Sinclair’s Approach For a Longer Life

David Sinclair wants to slow down and ultimately reverse aging. Sinclair sees aging as a disease and he is convinced aging is caused by epigenetic changes, abnormalities that occur when the body’s cells process extra or missing pieces of DNA. This results in the loss of the information that keeps our cells healthy. This information also tells the cells which genes to read. David Sinclair’s book: “Lifespan, why we age and why we don’t have to”, he describes the results of his research, theories and scientific philosophy as well as the potential consequences of the significant progress in genetic technologies.

At present, researchers are only just beginning to understand the biological basis of aging even in relatively simple and short-lived organisms such as yeast. Sinclair however, makes a convincing argument for why the life-extension technologies will eventually offer possibilities of life prolongation using genetic engineering.

He and his team recently developed two artificial intelligence algorithms that predict biological age in mice and when they will die. This will pave the way for similar machine learning models in people.
The loss of epigenetic information is likely the root cause of aging. By analogy, If DNA is the digital information on a compact disc, then aging is due to scratches. What we are searching for, is the polish.

Every time a cell divides, the DNA strands at the ends of your chromosomes replicate in order to copy all the genetic information to each new cell, and this process is not perfect. Over time, however, the ends of your chromosomes can become scrambled.

However, the progress in genetic engineering has proved that these changes can be reversed even at the cellular level, and it is possible to restore the information in our cells, thus improving the functioning of our organs and slowing the aging process.

#Aging #DavidSinclair #Lifespan

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A Genetic Variant That Protects Against Alzheimer’s Promotes Immune Cell Functions

Summary: PLCG2-P522R, a genetic variant that protects against Alzheimer’s disease, enhances key functions of immune cells.

Source: University of Eastern Finland

A new study conducted by researchers at the University of Eastern Finland found that the PLCG2-P522R genetic variant, which protects against Alzheimer’s disease, enhances several key functions of immune cells. The results obtained in the study highlight the importance of immune cells as a target of future development of new therapies for Alzheimer’s disease.

Neanderthal and Denisovan Y Chromosomes Sequenced – Surprise When Compared to Modern Human DNA

Neanderthals have adopted male sex chromosome from modern humans.

In 1997, the very first Neanderthal DNA sequence — just a small part of the mitochondrial genome — was determined from an individual discovered in the Neander Valley, Germany, in 1856. Since then, improvements in molecular techniques have enabled scientists at the Max Planck Institute for Evolutionary Anthropology to determine high quality sequences of the autosomal genomes of several Neanderthals, and led to the discovery of an entirely new group of extinct humans, the Denisovans, who were relatives of the Neanderthals in Asia.

However, because all specimens well-preserved enough to yield sufficient amounts of DNA have been from female individuals, comprehensive studies of the Y chromosomes of Neanderthals and Denisovans have not yet been possible. Unlike the rest of the autosomal genome, which represents a rich tapestry of thousands of genealogies of any individual’s ancestors, Y chromosomes have a peculiar mode of inheritance — they are passed exclusively from father to son. Y chromosomes, and also the maternally-inherited mitochondrial DNA, have been extremely valuable for studying human history.

160 Genes Linked to Brain Shrinkage in Study of 45,000 Adults

Researchers have identified 160 genes linked to brain shrinkage in adults. The genes appear to be involved in brain development, vascular and neurodegenerative diseases, and some psychiatric conditions.0 genes linked to brain shrinkage in adults. The genes appear to be involved in brain development, vascular and neurodegenerative diseases, and some psychiatric conditions.0 genes linked to brain shrinkage in adults. The genes appear to be involved in brain development, vascular and neurodegenerative diseases, and some psychiatric conditions.

Epigenetic Clocks: Which Has The Best Correlation For Aging and Age-Related Diseases?

11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.

University Obtains New Patent for Poison Ivy, Oak Vaccine

Circa 2019

OXFORD, Miss. – The University of Mississippi has been issued its fourth patent for a product that could prevent the painful itching and rash due to exposure to poison ivy, poison oak and poison sumac.

The compound is based on research conducted in the UM School of Pharmacy and at ElSohly Laboratories Inc. Hapten Sciences, a Memphis-based biopharmaceutical company, obtained a worldwide, exclusive license for the technology from the university in 2010 and has conducted extensive preclinical and clinical development work since then.

“We are delighted to be a partner with the University of Mississippi to develop this novel and important product candidate, and look forward to continued development to seek regulatory approval so that we can provide it to people that suffer from contact dermatitis caused by poison ivy, oak and sumac,” said Raymond J. Hage Jr., CEO and president of Hapten Sciences.

Humans live much longer than chimps due to a slower epigenetic ‘clock’

Lil bits of info on DNA methylation, clocks.

Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7–8 million years ago when our ancestors branched away from the lineage of chimps.

Slower ticker

There are tens of thousands of genes in the human genome, but that doesn’t mean all of them are active. For instance, through the methylation of DNA across certain sites of the genetic sequence, genes are locked in the “off” position. These modifications, known as epigenetic changes (‘epi’ means ‘above’ in Greek), do not alter the DNA sequence itself but, rather, simply regulate the activity of genes.

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