Lifeboat Foundation

Taking advantage of powerful advances in CRISPR gene editing, scientists at the University of California San Diego have set their sights on one of society’s most formidable threats to human health.

A research team led by Andrés Valderrama at UC San Diego School of Medicine and Surashree Kulkarni of the Division of Biological Sciences has developed a new CRISPR-based gene-drive system that dramatically increases the efficiency of inactivating a gene rendering bacteria antibiotic-resistant. The new system leverages technology developed by UC San Diego biologists in insects and mammals that biases genetic inheritance of preferred traits called “active genetics.” The new “pro-active” genetic system, or Pro-AG, is detailed in a paper published December 16 in Nature Communications.

Widespread prescriptions of antibiotics and use in animal food production have led to a rising prevalence of antimicrobial resistance in the environment. Evidence indicates that these environmental sources of antibiotic resistance are transmitted to humans and contribute to the current health crisis associated with the dramatic rise in drug-resistant microbes. Health experts predict that threats from antibiotic resistance could drastically increase in the coming decades, leading to some 10 million drug-resistant disease deaths per year by 2050 if left unchecked.

As part of the LEAF Longevity Bookclub and to celebrate the launch of Dr. David Sinclair’s new book, Lifespan: Why We Age and Why We Don’t Have To, we hosted a special webinar on the 18th of September. The new book takes us on a journey through the biology of why we age and spotlights the exciting research being done in the lab today which could potentially change the way we treat the diseases of aging.

Continue reading “Dr. David Sinclair Webinar – Lifespan: Why We Age – and Why We Don’t Have To” »

Carnegie Mellon University computer scientists have taken a deep learning method that has revolutionized face recognition and other image-based applications in recent years and redirected its power to explore the relationship between genes.

The trick, they say, is to transform massive amounts of gene expression data into something more image-like. Convolutional neural networks (CNNs), which are adept at analyzing visual imagery, can then infer which genes are interacting with each other. The CNNs outperform existing methods at this task.

The researchers’ report on how CNNs can help identify disease-related genes and developmental and genetic pathways that might be targets for drugs is being published today in the Proceedings of the National Academy of Science. But Ziv Bar-Joseph, professor of computational biology and machine learning, said the applications for the new method, called CNNC, could go far beyond gene interactions.

Humans have a maximum natural lifespan of only 38 years, according to researchers, who have discovered a way to estimate how long a species lives based on its DNA.

Scientists at Australia’s national science agency have developed a genetic ‘clock’ computer model that they claim can accurately estimate how long different vertebrates are likely to survive — including both living and extinct species.

Continue reading “Humans are genetically hardwired to only live for 38 YEARS” »

Is a film based on a video game with fleeting mentions of a biotech buzzword compelling sci-fi? No. But I liked Rampage anyway.

The use of CRISPR to edit genes is perhaps the only novel plot point in this latest monster movie. An evil head of a biotech company subverts a scientist’s work to fashion a bioweapon that revs up the growth hormone gene, and more, in three unfortunate animals. Cue Godzilla, King Kong, and the beast in Lake Placid.

But the screenwriters seem to confuse gene editing with an infectious bioweapon, like anthrax. The tagline at IMDb reveals the befuddlement: “When three different animals become infected with a dangerous pathogen, a primatologist and a geneticist team up to stop them from destroying Chicago.” Infectious disease, genetic modification, or both?

The idea of a cell therapy for Parkinson’s disease starts out simple: Symptoms of the progressive disease are largely driven by the deaths of dopamine-producing neurons found deep within the brain. With lower levels of the neurotransmitter come the characteristic tremors, rigidity and slow movements.

By replacing those lost nerve cells with new dopamine producers, researchers hope to renew the brain’s connection to the body’s muscles and improve a person’s overall motor function.

But in the brain, everything becomes more complicated. On top of the risk of immune system rejection that comes with any kind of living tissue transplant, it’s important to make sure the implanted cells function correctly and do not pick up any dangerous genetic mutations as they grow.

O.,o.

Acknowledges the fact that the Greys are cross-breeding with human beings in an attempt to re-vitalize the genetic structure of their species.

Using a targeted gene epigenome editing approach in the developing mouse brain, Johns Hopkins Medicine researchers reversed one gene mutation that leads to the genetic disorder WAGR syndrome, which causes intellectual disability and obesity in people. This specific editing was unique in that it changed the epigenome—how the genes are regulated—without changing the actual genetic code of the gene being regulated.

The researchers found that this gene, C11orf46, is an important regulator during brain development. Specifically, it turns on and off the direction-sensing proteins that help guide the long fibers growing out of newly formed neurons responsible for sending electrical messages, helping them form into a bundle, which connects the two hemispheres of the brain. Failure to properly form this bundled structure, known as the corpus callosum, can lead to conditions such as intellectual disability, autism or other brain developmental disorders.

“Although this work is early, these findings suggest that we may be able to develop future epigenome editing therapies that could help reshape the neural connections in the brain, and perhaps prevent developmental disorders of the brain from occurring,” says Atsushi Kamiya, M.D., Ph.D., associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.

A ketone-supplemented diet may protect neurons from death during the progression of Alzheimer’s disease, according to research in mice recently published in JNeurosci.

Early in the development of Alzheimer’s disease, the brain becomes over excited, potentially through the loss of inhibitory, or GABAergic, interneurons that keep other neurons from signaling too much. Because interneurons require more energy compared to other neurons, they may be more susceptible to dying when they encounter the Alzheimer’s disease protein amyloid beta. Amyloid beta has been shown to damage mitochondria — the metabolic engine for cells — by interfering with SIRT3, a protein that preserves mitochondrial functions and protects neurons.

Cheng et al. genetically reduced levels of SIRT3 in mouse models of Alzheimer’s disease. Mice with low levels of SIRT3 experienced a much higher mortality rate, more violent seizures, and increased interneuron death compared to the mice from the standard Alzheimer’s disease model and control mice. However, the mice with reduced levels of SIRT3 experienced fewer seizures and were less likely to die when they ate a diet rich in ketones, a specific type of fatty acid. The diet also increased levels of SIRT3 in the mice.