Lifeboat Foundation

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.

A ransomware attack on IT service vendor Virtual Care Provider has disrupted care at about 110 nursing homes and acute care facilities, locking the providers out of their patient records.

Inspired by their use in mechanical systems, Massachusetts Institute of Technology researchers are testing a magnetically-actuated fluidic valve to use in trauma patients suffering from hemorrhage.

Yonatan Tekleab and his colleagues will explain how the valve works at the American Physical Society’s Division of Fluid Dynamics 72nd Annual Meeting on Nov. 25 at the Washington State Convention Center in Seattle. The talk is part of a larger session on biological fluid dynamics for medical devices.

Approximately 80% of trauma related deaths after the first hour of admission to the hospital are due to hemorrhagic shock. Tekleab said their system of an injectable magnetorheological suspension and externally placed small magnets would be able to significantly reduce bleeding before the patient is transported to the hospital.

NaNotics, in another breakthrough, is promising a new kind of medication, and suggests to have found a way to combat age related diseases; boldly going where no nanotech has gone before.

Lou Hawthorne of NaNotics, LLC opened his presentation at a recent longevity investor event using a clip from Star Trek that shows captain Kirk being giving a shot that restores him to his younger years.

“It’s tempting to assume it’s a drug, but what if the content of that syringe was something new?” NaNotics’ CEO Hawthorne asked. “NaNots are a new class of medicine. They are engineered to do just one thing and that’s the holy grail of medicine design, because most drugs do two things: something you want them to do, and something you don’t. In other words, side effects.”

Excerpt of Brent Nally’s interview to Dr. Michael Fossel about his company Telocyte and telomerase gene therapy. The interview took place on November 16, 2019.

To watch the entire three and a half hour enlightening interview click here:

Continue reading “Michael Fossel on activating Telomerase as best single antiaging intervention” »

The relationship between health and the microorganisms living in the gut has increasingly reached the spotlight in the last few years, and a new study led by researchers at Nanyang Technological University, Singapore (NTU Singapore) sheds more light on the gut microbiome and how it can influence aging.

The gut microbiome

Continue reading “Gut Microbes Support Neurogenesis and Longevity Hormone Production” »

ERCC1 (excision repair cross complementing‐group 1) is a mammalian endonuclease that incises the damaged strand of DNA during nucleotide excision repair and interstrand cross‐link repair. Ercc1^−/Δ mice, carrying one null and one hypomorphic Ercc1 allele, have been widely used to study aging due to accelerated aging phenotypes in numerous organs and their shortened lifespan. Ercc1^−/Δ mice display combined features of human progeroid and cancer‐prone syndromes. Although several studies report cellular senescence and apoptosis associated with the premature aging of Ercc1^−/Δ mice, the link between these two processes and their physiological relevance in the phenotypes of Ercc1^−/Δ mice are incompletely understood. Here, we show that ERCC1 depletion, both in cultured human fibroblasts and the skin of Ercc1^−/Δ mice, initially induces cellular senescence and, importantly, increased expression of several SASP (senescence‐associated secretory phenotype) factors. Cellular senescence induced by ERCC1 deficiency was dependent on activity of the p53 tumor‐suppressor protein. In turn, TNFα secreted by senescent cells induced apoptosis, not only in neighboring ERCC1‐deficient nonsenescent cells, but also cell autonomously in the senescent cells themselves. In addition, expression of the stem cell markers p63 and Lgr6 was significantly decreased in Ercc1^−/Δ mouse skin, where the apoptotic cells are localized, compared to age‐matched wild‐type skin, possibly due to the apoptosis of stem cells. These data suggest that ERCC1‐depleted cells become susceptible to apoptosis via TNFα secreted from neighboring senescent cells. We speculate that parts of the premature aging phenotypes and shortened health‐ or lifespan may be due to stem cell depletion through apoptosis promoted by senescent cells.

A team from Cincinnati Children’s Hospital tracked stem cells injected into the hearts of mice, and what they found could explain why clinical trials testing stem cell therapies in people with heart disease have been unsuccessful. They believe a smarter approach could be to harness the power of macrophages that provide healing in response to inflammation.