Lifeboat Foundation

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.

My latest blood test results are in-how’s my biological age?

In the video I discuss my dietary approach prior to my latest blood test, the blood test results, and my plan to improve them going forward.

“Observations of metastasising cells revealed something intriguing—a high level of something called methylmalonic acid (MMA), a metabolic byproduct that appears to accumulate as we get older.”

“So how does MMA induce these changes in cancer cells? The key seems to be in a sort of reprogramming that “switches on” a gene called SOX4.

Prior research has shown SOX4 encourages cancer cells to become more aggressive and prone to metastasis.

Continue reading “Study finds cancer-boosting culprit that multiplies with age” »

Research is showing a strong link between handgrip strength, walking speed, and cognition, indicating how improved physical health could boost elderly minds.

Based at Barwon Health, in the heart of Geelong’s clinical health precinct, researchers are working to identify the risk factors —such as changes in muscle mass, muscle strength and physical performance—for developing sarcopenia (loss of muscle mass, strength and function with advancing age) across the lifespan.

This testing involves the Geelong Osteoporosis Study (GOS) which began in the early 1990s, gathering adult participants from the electoral roll in the Barwon Statistical Division. During recent follow-up testing, researchers also measured cognitive function through a computer-based program, in tandem with physical health evaluations.

For decades, greater than 60% of the human genome was believed to be “junk DNA” that served little or no purpose in the course of human development. Recent research by Colorado State University is challenging this notion to show that junk DNA might be important after all.

A new study, published on June 5 in Aging Cell, found that a portion of noncoding genetic material, called repetitive element transcripts, might be an important biomarker of the aging process.

Tom LaRocca, an assistant professor in the Department of Health and Exercise Science and faculty member in the Columbine Heath Systems Center for Healthy Aging at CSU, led the study to investigate a growing body of evidence that repetitive elements—transposons and other sequences that occur in multiple copies in the human genome —may become active over time as we age.

Aubrey interviewed by, um, alien scientists.

Our conversation covers the importance of non-academic institutions in science, strategies for combating for repair the damage of aging, and an exploration of how extending human lifespan will change the Earth. In Dr. de Gray’s perspective, age-related decline is a medical problem like any other that can be treated and cured by cutting edge technology. He’s devoted himself to this pursuit as a founder of the SENS Research Foundation, the Methuselah Foundation, and the medical startup AgeX.

Continue reading “A Future Without Aging — Dr. Aubrey de Grey” »

NR and NMN are popular ways to try to boost levels of NAD+, but that approach hasn’t worked every time in human studies. One reason for that may involve CD38, which degrades both NR and NMN. With the goal of boosting NAD+ levels during aging, why does CD38 increase with age, and what can be done about it? All that and more in this video!