Lifeboat Foundation

Salk Institute scientists have harnessed stem cell technology to generate the first human insulin-producing pancreatic cell clusters that can evade the immune system. Generated from induced pluripotent stem cells (iPSCs), these “immune shielded” human islet-like organoids (HILOs) controlled blood glucose following transplantation into a mouse model of diabetes, without the use of immunosuppressive drugs. The researchers suggest the achievement represents a major advance in the quest for a safe and effective treatment for type 1 diabetes (T1D), which impacts an estimated 1.6 million people in the United States, at a cost of $14.4 billion annually.

“Most type 1 diabetics are children and teenagers,” said Salk professor Ronald Evans, PhD, holder of the March of Dimes chair in molecular and developmental biology. Evans is senior author of the team’s paper, which is published in Nature. “This is a disease that is historically hard to manage with drugs. We hope that regenerative medicine in combination with immune shielding can make a real difference in the field by replacing damaged cells with lab-generated human islet-like cell clusters that produce normal amounts of insulin on demand.”

Continue reading “Diabetes Controlled in Mice Using First Immune-Evading Human Islet Cell Organoids” »

We are witnessing the birth of a new faith. It is not a theistic religion. Indeed, unlike Christianity, Judaism, and Islam, it replaces a personal relationship with a transcendent God in the context of a body of believers with a fervent and radically individualistic embrace of naked materialistic personal recreation.

Moreover, in contrast to the orthodox Christian, Judaic, and Islamic certainty that human beings are made up of both material body and immaterial soul – and that both matter – adherents of the new faith understand that we have a body, but what really counts is mind, which is ultimately reducible to mere chemical and electrical exchanges. Indeed, contrary to Christianity’s view of an existing Heaven or, say, Buddhism’s conception of the world as illusion, the new faith insists that the physical is all that has been, is, or ever will be.

Such thinking leads to nihilism. That’s where the new religion leaves past materialistic philosophies behind, by offering adherents hope. Where traditional theism promises personal salvation, the new faith offers the prospect of rescue via radical life-extension attained by technological applications – a postmodern twist, if you will, on faith’s promise of eternal life. This new religion is known as “transhumanism,” and it is all the rage among the Silicon Valley nouveau riche, university philosophers, and among bioethicists and futurists seeking the comforts and benefits of faith without the concomitant responsibilities of following dogma, asking for forgiveness, or atoning for sin – a foreign concept to transhumanists. Truly, transhumanism is a religion for our postmodern times.

“Using microfluidics, computer modeling and other techniques, they found that about half of the cells age through a gradual decline in the stability of the nucleolus, a region of nuclear DNA where key components of protein-producing “factories” are synthesized,” a press release announcing the research explains. “In contrast, the other half age due to dysfunction of their mitochondria, the energy production units of cells.”

Researchers studying aging have discovered that cells tend to follow one of two aging pathways. The way each individual cell ages is determined early on, and scientists can predict how a cell will age based on early observations.

If you eschew hyperbole and hang in for the long haul, maintaining a discipline of understatement in the midst of a flashy neon world, you may be offered a modicum of credence when you make an extraordinary announcement. No one is entitled to this courtesy twice. If the news that you trumpet to the moon does not pan out, your readers will be justified in discounting everything you say thereafter.

Here goes.

Continue reading “Age Reduction Breakthrough” »

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How we adapt to aging late in life may be genetically influenced, according to a study led by a psychologist at the University of California, Riverside.

The research, published in Aging Cell, has implications for how epigenetic factors relate to aging. Epigenesis is a process in which chemicals attached to DNA control its activity. Epigenetic changes, which can be passed on to offspring, may be critical to accelerated aging as well as declines in cognitive and physical functioning that often accompany aging. Epigenetic modifications resulting in altered gene expression may occur due to a number of biological processes, including one the researchers focused on: DNA methylation.

In DNA methylation, methyl groups are added to the DNA molecule. DNA has four different types of nucleotides: A, T, G, and C. DNA methylation occurs at the C bases of eukaryotic DNA. Changes in DNA methylation correlate strongly with aging.

Most of us are now familiar with apps that track what’s known as our ‘digital biomarkers’. These include the steps, we’ve taken, our heart rate, and our weight. In recent years startups have appeared which can, in a relatively turnkey manner, track our ‘biomedical markers’, such as cholesterol levels, for instance. Few, however, are seeking to combine the two to get a 360-degree view of how our bodies are doing.

Into this gap steps Humanity Inc., which will seek to do exactly that. Founded by two seasoned entrepreneurs, Humanity will combine digital and biomedical biomarkers into a consumer app that will fully launch next year.

Today it announces it’s initial seed fundraise of $2.5m, in a round led by Boston fund One Way Ventures and the legendary and long-time HealthTech Angel investor Esther Dyson, among others.

Summary: Researchers identified a group of closely related genes that capture molecular links between Alzheimer’s and LATE, a common brain disorder that mimics Alzheimer’s symptoms.

Source: Brigham and Women’s Hospital

Alzheimer’s disease is one of the most common causes of dementia, and while most people might know someone who is affected by it, the genetic factors behind the disease are less known. A new study by investigators from Brigham and Women’s Hospital uncovered a group of closely related genes that may capture molecular links between Alzheimer’s disease and Limbic-predominant Age-related TDP-43 Encephalopathy, or LATE, a recently recognized common brain disorder that can mimic Alzheimer’s symptoms. LATE is often combined with Alzheimer’s disease to cause a more rapid cognitive decline. The study’s results are published in Neuron.

Scientists investigating Alzheimer’s treatments at the Salk Institute have uncovered some key mechanisms that enable an experimental drug to reverse memory loss in mouse models of the disease. The discovery not only bodes well for the possibility of clinical trials, but provides researchers with a new target to consider in the wider development of compounds to counter the degenerative effects of the condition.

The research centers on a drug called CMS121, which is a synthetic version of a chemical called fisetin that occurs naturally in fruits and vegetables. The Salk team’s previous studies concerning CMS121 have produced some very promising results, with one paper published last year describing how the drug influences age-related metabolic pathways in the brain, protecting against the type of degeneration associated with Alzheimer’s. This followed earlier studies demonstrating how fisetin can prevent memory loss in mice engineered to develop Alzheimer’s.

Work continues at Salk to understand how exactly fisetin and the synthetic variant CMS121 produces these anti-aging effects on the brain. In their latest study, the researchers again turned to mice engineered to develop Alzheimer’s, which were administered daily doses of CMS121 from the age of nine months. This is the equivalent to middle age in humans, with the mice already exhibiting learning and memory problems before the treatment began.