Lifeboat Foundation

Dr Ian Pearson warns ‘electronic immortality’ will require careful planning. It could mean we live on after death in an ‘upgraded body’ — but could also mean we no longer own our own minds.

A new study shows that mice reprogram their gut tissues to repair injury rolling them from an aged state back to a more fetal-like one.

Getting old is one thing; getting old in a healthy way is another. Many elderly people suffer from all kinds of diseases and disorders, ranging from cardiovascular problems and diabetes to Alzheimer’s and Parkinson’s disease. Wouldn’t it be nice if we could keep the body young as we grow older to prevent disease associated with old age? For instance, would it be possible to slow down or reverse the aging processes in the cells of our body?

This question has gained a lot of interest from scientists, and their research has led to the discovery of the important role that the shortening of telomeres, the protective caps on our DNA, plays in aging. While this has been described in recent posts on the LEAF blog, I would like to address another mechanism that has seen an interesting leap forward, more or less by accident: rejuvenation of tissue.

Continue reading “Mice Reprogram Gut Tissue to a Fetal State to Heal Injury” »

Who wants to live forever? Thanks to these scientific breakthroughs, increased lifespans and reverse aging could be possible.

Aging may seem like the most natural—and inevitable—thing in life. Yet according to a new study in Nature Medicine, rejuvenating an aging body may be as easy as kitchen renovations. Simply swap drill and hammer for a cocktail of two drugs already on the market; rather than pulling out decrepit cabinets, kill off aged “zombie” cells.

These so-called senescent cells are a curious oddity: they’re frail, beat-up, and unable to perform their usual roles. Yet they simply refuse to die. What’s more, zombie cells actively leak inflammatory chemicals into their surroundings, damaging nearby tissue and—in a sense—“spreading” the negative effects of aging.

Yet because they’re extremely rare, amounting to only eight percent of the body’s cells at most, scientists have long wondered just how much they contribute to the aging process.

Continue reading “This Drug Combo Extends Lifespan and Healthspan in Mice” »

It was a major feature for the #transhumanism and life extension movements, seen by likely millions of people because it was translated into various languages via international syndication. Story by Richard Godwin. https://www.thetimes.co.uk/article/zoltan-istvan-the-poster-…-lrbx66lqn

Aging may be regulated by a discrete set of intracellular proteins including the mechanistic target of rapamycin (mTOR) kinase. mTOR functions within two multiprotein complexes called TORC1 and TORC2. Inhibition of TORC1 has extended life span in every species studied to date and ameliorated multiple aging-related pathologies including declining immune function. Mannick et al. now show that low-dose TORC1 inhibitor therapy in elderly humans decreased the incidence of all infections, improved influenza vaccination responses, and up-regulated antiviral immunity. Thus, targeting the TORC1 pathway that regulates aging may have clinical benefits for elderly humans including improvement in immune function and decreased infection rates.

Inhibition of the mechanistic target of rapamycin (mTOR) protein kinase extends life span and ameliorates aging-related pathologies including declining immune function in model organisms. The objective of this phase 2a randomized, placebo-controlled clinical trial was to determine whether low-dose mTOR inhibitor therapy enhanced immune function and decreased infection rates in 264 elderly subjects given the study drugs for 6 weeks. A low-dose combination of a catalytic (BEZ235) plus an allosteric (RAD001) mTOR inhibitor that selectively inhibits target of rapamycin complex 1 (TORC1) downstream of mTOR was safe and was associated with a significant (P = 0.001) decrease in the rate of infections reported by elderly subjects for a year after study drug initiation. In addition, we observed an up-regulation of antiviral gene expression and an improvement in the response to influenza vaccination in this treatment group.

In a study on murine mtDNA, scientists reversed skin wrinkles and hair loss.

In what appears to be a world first, scientists at the University of Alabama at Birmingham have reversed two of the most common visual signs of aging—skin wrinkles and hair loss—in mice by turning off a gene responsible for mitochondrial dysfunction [1].

Study abstract

Continue reading “Intervening on mtDNA in Mice Reverses Skin Wrinkling and Hair Loss” »

Australian researchers have made a discovery about telomeres that may have implications for aging, heart disease, cancer, and other age-related diseases.

So, what are telomeres?

Each of the chromosomes that store our genetic information has a telomere at each end. This protective cap consists of a specific DNA sequence that is repeated thousands of times and has two purposes: firstly, it protects the coding regions of the chromosomes and prevents them from being damaged, and secondly, it acts as a clock that controls the number of replications a cell can undergo; this is thought to act as a quality control system to ensure that aged and potentially damaged cells do not remain in circulation.

BIRMINGHAM, Ala. — Wrinkled skin and hair loss are hallmarks of aging. What if they could be reversed?

Keshav Singh, Ph.D., and colleagues have done just that, in a mouse model developed at the University of Alabama at Birmingham. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks. When the mitochondrial function is restored by turning off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age.

“To our knowledge, this observation is unprecedented,” said Singh, a professor of genetics in the UAB School of Medicine.