The pharmaceuticals firm GSK has struck a five-year partnership with King’s College London to use artificial intelligence to develop personalised treatments for cancer by investigating the role played by genetics in the disease.
The tie-up, which involves 10 of the drug maker’s artificial intelligence experts working with 10 oncology specialists from King’s across their labs, will use computing to “play chess with cancer”, working out why only a fifth of patients respond well to immuno-oncology treatments.
CRISPR technology offers the promise to cure any human genetic disease with gene editing; which one will be the first?
CRISPR-Cas9 was first used as a gene-editing tool in 2012. In just a few years, the technology has exploded in popularity thanks to its promise of making gene editing much faster, cheaper, and easier than ever before.
CRISPR is short for ‘clustered regularly interspaced short palindromic repeats.’ The term makes reference to a series of repetitive patterns found in the DNA of bacteria that form the basis of a primitive immune system, defending them from viral invaders by cutting their DNA.
Ancient DNA extracted from human bones has rewritten early Japanese history by underlining that modern day populations in Japan have a tripartite genetic origin—a finding that refines previously accepted views of a dual genomic ancestry.
Twelve newly sequenced ancient Japanese genomes show that modern day populations do indeed show the genetic signatures of early indigenous Jomon hunter-gatherer-fishers and immigrant Yayoi farmers—but also add a third genetic component that is linked to the Kofun peoples, whose culture spread in Japan between the 3rd and 7th centuries.
He explored the possibility of using gene therapy or gene editing—technologies that were dominating headlines for their ability to tackle other rare genetic disorders. But scientists told him those approaches would be difficult to implement for Dravet. Instead, a newfangled idea called transfer RNA (tRNA) therapy seemed like it might be the answer.
Drug Discovery tRNA therapies could help restore proteins lost in translation.
A new class of therapies based on transfer RNA could treat forms of cystic fibrosis, muscular dystrophy, genetic epilepsies, and more by.
This is the video of Harold Katcher’s presentation to the London Futurists. It was a great discussion, be sure to check it out.
#haroldkatcher #antiaging #rejuvenation #futurism
It has been known for some time that young blood plasma can confer beneficial effects on various organs in mice, although the mechanisms and implications remained unclear. A recent breakthrough experiment is attracting more attention to this area of research: rats treated with a blood plasma mixture known as E5 subsequently had their effective biological age measured by epigenetic clocks, involving 593 tissue samples. The result was a halving of the epigenetic ages of blood, heart, and liver tissue, and a lesser reduction (still statistically significant) in the epigenetic age of the hypothalamus. This has been heralded as the single most dramatic age-reversal experiment in mammals to date.
On Saturday 18th September, the lead designer of these experiments, Dr Harold Katcher, joined London Futurists to present his analysis of the findings, his own distinctive theories of aging, and his expectation for future research and applications. He also answered questions about his new book, “The Illusion of Knowledge: The paradigm shift in aging research that shows the way to human rejuvenation”, which is available at https://www.amazon.co.uk/Illusion-Knowledge-paradigm-researc…09C7JNB64/
The event was introduced and moderated by David Wood, Chair of London Futurists.
A bioengineer and geneticist at Harvard’s Wyss Institute have successfully stored 5.5 petabits of data — around 700 terabytes — in a single gram of DNA, smashing the previous DNA data density record by a thousand times.
The work, carried out by George Church and Sri Kosuri, basically treats DNA as just another digital storage device. Instead of binary data being encoded as magnetic regions on a hard drive platter, strands of DNA that store 96 bits are synthesized, with each of the bases (TGAC) representing a binary value (T and G = 1 A and C = 0).
To read the data stored in DNA, you simply sequence it — just as if you were sequencing the human genome — and convert each of the TGAC bases back into binary. To aid with sequencing, each strand of DNA has a 19-bit address block at the start (the red bits in the image below) — so a whole vat of DNA can be sequenced out of order, and then sorted into usable data using the addresses.
“You may hit the tipping point when you’re 50; it may happen when you’re 80; it may never happen,” Schindler said. “But once you pass the tipping point, you’re going to accumulate high levels of amyloid that are likely to cause dementia. If we know how much amyloid someone has right now, we can calculate how long ago they hit the tipping point and estimate how much longer it will be until they are likely to develop symptoms.”
Summary: A new algorithm uses neuroimaging data of amyloid levels in the brain and takes into account a person’s age to determine when a person with genetic Alzheimer’s risk factors, and with no signs of cognitive decline, will develop the disease.
Source; WUSTL
Researchers at Washington University School of Medicine in St. Louis have developed an approach to estimating when a person who is likely to develop Alzheimer’s disease, but has no cognitive symptoms, will start showing signs of Alzheimer’s dementia.
The algorithm, available online in the journal Neurology, uses data from a kind of brain scan known as amyloid positron emission tomography (PET) to gauge brain levels of the key Alzheimer’s protein amyloid beta.
Replacing or editing disease-causing mutations holds great promise for treating many human diseases. Yet, delivering therapeutic genetic modifiers to specific cells in vivo has been challenging, particularly in large, anatomically distributed tissues such as skeletal muscle. Here, we establish an in vivo strategy to evolve and stringently select capsid variants of adeno-associated viruses (AAVs) that enable potent delivery to desired tissues. Using this method, we identify a class of RGD motif-containing capsids that transduces muscle with superior efficiency and selectivity after intravenous injection in mice and non-human primates. We demonstrate substantially enhanced potency and therapeutic efficacy of these engineered vectors compared to naturally occurring AAV capsids in two mouse models of genetic muscle disease. The top capsid variants from our selection approach show conserved potency for delivery across a variety of inbred mouse strains, and in cynomolgus macaques and human primary myotubes, with transduction dependent on target cell expressed integrin heterodimers.
The label on RecA together with fluorescent markers on the DNA allows the researchers to follow every step of the process accurately; for example, they conclude that the whole repair is finished in 15 minutes, on average, and that the template is located in about nine. Using microscopy, Elf and his team investigate the fate of the break site and its homologous copy in real-time. They also find that the cell responds by rearranging RecA to form thin filaments that span the length of the cell.
How the cell can mend broken DNA
DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).