Lifeboat Foundation

If you’ve ever worked with a virtualized computer, or played a video game ROM from a long-defunct console on your new PC, you understand the concept already: a mind is simply software, and the brain, the hardware it runs on. Imagine a day when your neurons, the matter that forms your mind, are transferred to a machine and their counterparts in your skull are disabled.

Are you still you? Imagine a future of mind uploading, whole-brain emulation, and the full understanding of the connectome. Now, imagine neuroscientists even discover a way to resurrect the dead, to upload the mind of those who have gone before, our ancestors, Socrates, Einstein?

In a paper published in Plos One in early December, scientists detailed how they were able to elicit a pattern similar to the living condition of the brain when exposing dead brain tissue to chemical and electrical probes. Authors Nicolas Rouleau, Nirosha J. Murugan, Lucas W. E. Tessaro, Justin N. Costa, and Michael A. Persinger (the same Persinger of the God-Helmet studies) wrote about this breakthrough.

Since the dawn of time, humans have been trying to find a way to cheat death. Some researchers now believe they’re closer than ever to beating the ageing process and dramatically extending lives. Is immortality possible?
#immortality #ageing #liveforever

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H/T Dr. Jason Williams

Creatine, the organic acid that is popularly taken as a supplement by athletes and bodybuilders, serves as a molecular battery for immune cells by storing and distributing energy to power their fight against cancer, according to new UCLA research.

The study, conducted in mice and published in the Journal of Experimental Medicine, is the first to show that creatine uptake is critical to the anti-tumor activities of CD8 T cells, also known as killer T cells, the foot soldiers of the immune system. The researchers also found that creatine supplementation can improve the efficacy of existing immunotherapies.

“Because oral creatine supplements have been broadly utilized by bodybuilders and athletes for the past three decades, existing data suggest they are likely safe when taken at appropriate doses,” said Lili Yang, a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and the study’s senior author. “This could provide a clear and expedient path forward for the use of creatine supplementation to enhance existing cancer immunotherapies.”

University of Southern California scientist Valter Longo talks in this Q&A about fasting and the adoption of a “longevity diet.” A researcher focusing on intermittent fasting and aging, Longo advocates a plant-based diet and smart, strategic caloric restriction for a longer, healthier life.

Neumann et al. demonstrate that aging renders adult oligodendrocyte progenitor cells unresponsive to pro-differentiation factors, which can be reversed both in vitro and in vivo by calorie restriction (CR) and the CR mimetic metformin.

A chance finding 10 years ago led to the creation by researchers of the Spanish National Cancer Research Centre (CNIO) of the first mice born with much longer telomeres than normal in their species. Telomeres shorten throughout life, so older organisms have shorter telomeres. Given this relationship between telomeres and aging, the scientists launched a study generating mice in which 100 percent of their cells had hyper-long telomeres. The findings are published in Nature Communications and show only positive consequences: The animals with hyper-long telomeres live longer and in better health, free from cancer and obesity. This marks the first time that longevity has been significantly increased without any genetic modification.

“This finding supports the idea that, when it comes to determining longevity, genes are not the only thing to consider,” says Maria Blasco, head of the CNIO Telomeres and Telomerase Group and intellectual author of the paper. “There is margin for extending life without altering the genes.”

Telomeres form the ends of chromosomes in the nucleus of each cell in the body. Their function is to protect the integrity of the genetic information in DNA. Whenever the cells divide the telomeres, they are slightly shortened, so one of the main characteristics of aging is the accumulation of shorter telomeres in cells. “Telomere shortening is considered to be one of the primary causes of aging, given that short telomeres cause aging of the organism and reduce longevity,” the authors write in a paper published in Nature Communications.

Dessie is a hundred years old.

By most standards this is a ripe old age, one most of us would be grateful to be given. Assuming our health remained decent, most of us would be content to live for seventy or eighty years.

Help Them See the Future, a joint venture between Integrated Health Systems and Maximum Life Foundation, created a campaign to give Dessie gene therapies designed to halt or potentially reverse some of the hallmarks of aging. We are sad to announce that, after suffering a stroke shortly after the campaign was launched, Dessie is no longer a suitable candidate for treatment.

The blind mole rat (Spalax) is a wild, long‐lived rodent that has evolved mechanisms to tolerate hypoxia and resist cancer. Previously, we demonstrated high DNA repair capacity and low DNA damage in Spalax fibroblasts following genotoxic stress compared with rats. Since the acquisition of senescence‐associated secretory phenotype (SASP) is a consequence of persistent DNA damage, we investigated whether cellular senescence in Spalax is accompanied by an inflammatory response. Spalax fibroblasts undergo replicative senescence (RS) and etoposide‐induced senescence (EIS), evidenced by an increased activity of senescence‐associated beta‐galactosidase (SA‐β‐Gal), growth arrest, and overexpression of p21, p16, and p53 mRNAs. Yet, unlike mouse and human fibroblasts, RS and EIS Spalax cells showed undetectable or decreased expression of the well‐known SASP factors: interleukin‐6 (IL6), IL8, IL1α, growth‐related oncogene alpha (GROα), SerpinB2, and intercellular adhesion molecule (ICAM‐1). Apparently, due to the efficient DNA repair in Spalax, senescent cells did not accumulate the DNA damage necessary for SASP activation. Conversely, Spalax can maintain DNA integrity during replicative or moderate genotoxic stress and limit pro‐inflammatory secretion. However, exposure to the conditioned medium of breast cancer cells MDA‐MB‐231 resulted in an increase in DNA damage, activation of the nuclear factor κB (NF‐κB) through nuclear translocation, and expression of inflammatory mediators in RS Spalax cells. Evaluation of SASP in aging Spalax brain and intestine confirmed downregulation of inflammatory‐related genes. These findings suggest a natural mechanism for alleviating the inflammatory response during cellular senescence and aging in Spalax, which can prevent age‐related chronic inflammation supporting healthy aging and longevity.

Short telomeres trigger age-related pathologies and shorter lifespans in mice and humans. In the past, we generated mouse embryonic (ES) cells with longer telomeres than normal (hyper-long telomeres) in the absence of genetic manipulations, which contributed to all mouse tissues. To address whether hyper-long telomeres have deleterious effects, we generated mice in which 100% of their cells are derived from hyper-long telomere ES cells. We observe that these mice have longer telomeres and less DNA damage with aging. Hyper-long telomere mice are lean and show low cholesterol and LDL levels, as well as improved glucose and insulin tolerance. Hyper-long telomere mice also have less incidence of cancer and an increased longevity. These findings demonstrate that longer telomeres than normal in a given species are not deleterious but instead, show beneficial effects.