Lifeboat Foundation

This is an excerpt of a conversation between Dr. Daniel Stickler and Brian Rose.
Dr. Stickler is the Medical Director for the Neurohacker Collective, a consultant for Google on epigenetics and AI in healthcare, and a lecturer at Stanford University.
Brian Rose is the founder of London Real, a curator of people worth watching. Its mission is to promote personal transformation through inspiration, self-discovery and empowerment.
CUENTA CON SUBTÍTULOS EN ESPAÑOL
To watch the entire conversation clic here: https://youtu.be/ynbaJ2038K0

Could speed up healing.

Wound healing in mammalian skin often results in fibrotic scars, and the mechanisms by which original nonfibrotic tissue architecture can be restored are not well understood. Here, Wei et al. have shown that pharmacological activation of the nociceptor TRPA1, which is found on cutaneous sensory neurons, can limit scar formation and promote tissue regeneration. They confirmed the efficacy of TRPA1 activation in three different skin wounding mouse models, and they also observed that localized activation could generate a response at distal wound sites. TRPA1 activation induced IL-23 production by dermal dendritic cells, which activated IL-17–producing γδ T cells and promoted tissue regeneration. These findings provide insight into neuroimmune signaling pathways in the skin that are critical to mammalian tissue regeneration.

Adult mammalian wounds, with rare exception, heal with fibrotic scars that severely disrupt tissue architecture and function. Regenerative medicine seeks methods to avoid scar formation and restore the original tissue structures. We show in three adult mouse models that pharmacologic activation of the nociceptor TRPA1 on cutaneous sensory neurons reduces scar formation and can also promote tissue regeneration. Local activation of TRPA1 induces tissue regeneration on distant untreated areas of injury, demonstrating a systemic effect. Activated TRPA1 stimulates local production of interleukin-23 (IL-23) by dermal dendritic cells, leading to activation of circulating dermal IL-17–producing γδ T cells. Genetic ablation of TRPA1, IL-23, dermal dendritic cells, or γδ T cells prevents TRPA1-mediated tissue regeneration.

Here’s my latest video!

The incidence of fungi bloodstream infections increases during aging-is that a potential explanation for the presence of fungi in the brains of Alzheimer’s disease patients? Rapamycin is a known antifungal-is it effective against fungi that are found in the blood and brain?

Very interesting.

Despite the limited supply of organs available for patients on waitlists for transplantation, organs from older, deceased donors are frequently discarded or not utilized. Available older organs have the potential to close the gap between demand and supply that is responsible for the very long wait-times that lead to many patients not surviving the time it takes for an organ to become available. Older organs can also often provoke a stronger immune response and may put patients at greater risk of adverse outcomes and transplant rejection. But, as the world population ages, organs from older, deceased donors represent an untapped and growing resource for patients in need. Investigators from Brigham and Women’s Hospital are leading efforts to breathe new life into older organs by leveraging a new class of drugs known as senolytics, which target and eliminate old cells. Using clinical and experimental studies, the team presents evidence that senolytic drugs may help rejuvenate older organs, which could lead to better outcomes and a wider pool of organs eligible for donation. Results are published in Nature Communications.

“Older organs are available and have the potential to contribute to mitigating the current demand for organ transplantation,” said corresponding author Stefan G. Tullius, MD, Ph.D., chief of the Division of Transplant Surgery at the Brigham. “If we can utilize older organs in a safe way with outcomes that are comparable, we will take a substantial step forward for helping patients.”

Continue reading “Rejuvenating old organs could increase donor pool” »

Research looking at a possible new therapeutic approach for Alzheimer’s disease was recently published in the Journal of Neuroinflammation. The paper out of the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA) is titled “Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition”. The work looked at targeting inflammation by using an antibody. Alzheimer’s disease and related dementias have no disease-modifying treatments at this time and represent a looming public health crisis given the continually growing aging population.

The paper explains that current therapeutic approaches to the treatment of Alzheimer’s disease focus on the major pathological hallmarks of the disease which are amyloid plaques and neurofibrillary tangles. They are the requirements for a diagnosis of Alzheimer’s disease. However, the authors say there has been an explosion of genetic data suggesting the risk for sporadic Alzheimer’s disease is driven by several other factors including neuroinflammation, membrane turnover and storage, and lipid metabolism.

In this study the researchers focused on triggering receptor expressed on myeloid cell-2 (TREM2). “TREM2 was identified several years ago as a gene that, when there’s a mutation, significantly increases risk of Alzheimer’s disease. The field thinks that this mutation reduces the function of the receptor, so we hypothesized that targeting TREM2 to increase its function might be a valid treatment for Alzheimer’s,” explained Donna Wilcock, SBCoA associate director.

Dr. Shigeaki Hinohara had an extraordinary life for many reasons. For starters, the Japanese physician and longevity expert lived until the age of 105.

When he died, in 2017, Hinohara was chairman emeritus of St. Luke’s International University and honorary president of St. Luke’s International Hospital, both in Tokyo.

Perhaps best known for his book, “Living Long, Living Good,” Hinohara offered advice that helped make Japan the world leader in longevity. Some were fairly intuitive points, while others were less obvious:

The plastic tips attached to the ends of shoelaces keep them from fraying. Telomeres are repetitive DNA (deoxyribonucleic acid) sequences that serve a similar function at the end of chromosomes, protecting its accompanying genetic material against genome instability, preventing cancers and regulating the aging process.

Each time a cell divides in our body, the telomeres shorten, thus functioning like a molecular “clock” of the cell as the shortening increases progressively with aging. An accurate measure of the quantity and length of these telomeres, or “clocks,” can provide vital information if a cell is aging normally, or abnormally, as in the case of cancer.

To come up with an innovative way to diagnose telomere abnormalities, a research team led by Assistant Professor Cheow Lih Feng from the NUS Institute for Health Innovation & Technology (iHealthtech) has developed a novel method to measure the absolute telomere length of individual telomeres in less than three hours. This unique telomere profiling method can process up to 48 samples from low amounts (1 ng) of DNA.

Our muscles start to shrink and weaken when we reach our 50s and 60s in a process called sarcopenia, but new research in mice from the University of Michigan offers new insights into why this loss may occur, and how we might begin to prevent it.

Sarcopenia is the progressive loss of muscle mass in aging, and it’s linked to other age-related pathologies such as osteoarthritis, cardiovascular disease and cancer, as well as an overall reduction in function and independence.

The research, led by Carlos Aguilar, a U-M assistant professor of biomedical engineering, focused on muscle stem cells since they are dedicated solely to keeping muscles healthy. And to better understand stem cell function during aging, testing was conducted on two sets of mice, one “young” and one “old,” before and after muscle injury.

As best we can guess, life started on planet Earth about 3.5 billion years ago. Unfortunately, so did death. And the reaper remains undefeated.

About 99 percent of all species that ever lived are now extinct. There’s almost no scientific reason to believe humans won’t join them in a relatively insignificant amount of time. I say almost because, if we try really hard, we can conceive of a theoretical, science-based intervention for death. Let’s call it a “quantum respawn.”

We’re not the first generation to imagine immortality. But we are the first one to have access to this really cool research paper from physicists working at the University of Rochester in New York, and Purdue University in Indiana.