Lifeboat Foundation

While the social media company cooperated with the research, it tracks other findings that social ties are linked to longevity.

“Calorie restriction has been known to extend lifespan for a long time.” said Dr. Kennedy. “The DNA damage response is linked to aging as well. LOS1 may be connecting these different processes.”

A number of the age-extending genes the team identified are also found in C. elegans roundworms, indicating these mechanisms are conserved in higher organisms. In fact, many of the anti-aging pathways associated with yeast genes are maintained all the way to humans.

The research produced another positive result: exposing emerging scientists to advanced lab techniques, many for the first time.

SRF Summer Scholars Program opens December 1st!

The SRF Summer Scholars Program offers undergraduate students the opportunity to conduct biomedical research to combat diseases of aging, such as cancer, Alzheimer’s, and Parkinson’s Disease. Under the guidance of a scientific mentor, each Summer Scholar is responsible for his or her own research project in such areas as genetic engineering and stem cell research. The Summer Scholars Program emphasizes development of both laboratory and communication skills to develop well-rounded future scientists, healthcare professionals, and policy makers. Students participating in the program will hone their writing skills via periodic reports, which are designed to emulate text scientists commonly must produce. At the end of the summer, students will have the opportunity to put all of their newly developed communication skills into practice at a student symposium.

Continue reading “2017 SRF Summer Scholars Program” »

Aubrey de Grey in the British paper “The Express”. Sadly not given the his correct Dr. title and also misquoted once again as saying people will live forever.

HUMANS could potentially live forever, according to a a leading researcher on the subject.

2013 saw the release of one of the most important papers in aging research and one that saw renewed interest and support for the concept of SENS.

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.

The excellent SENS animations hosted by Edward James Olmos of battlestar galactica fame.

Discover how SENS Research Foundation is driving public and professional recognition of potential true cures for age-related diseases and disabilities.

A woman living on a dialysis machine is grown a new kidney using her own cells. A father struggling with age-related vision loss has his eyesight restored. A soldier suffers extensive burns and has his skin regenerated.

This is a glimpse of the holy grail of regenerative medicine. The ultimate goal of the field is to develop therapies that restore normal function to diseased tissues and organs. Advances in 3D bioprinting, the process of fabricating functional human tissue outside the body in a layer-by-layer fashion, have pushed the envelope on what is considered possible in the field.

Continue reading “Printable Organs Will Put an End to Transplant Lists” »

Dr. Watson will see you now…

IBM Watson is rapidly earning its place in medical diagnosis. It has recently proven its ability to accurately diagnose patients and far faster than conventional doctors could ever do. The world of diagnosis of medicine is going to change very rapidly in the next few years.

#crowdfundthecure #aging

Continue reading “Dr House goes digital as IBM’s Watson diagnoses rare diseases” »

More news on senolytics.

Efforts to build rejuvenation therapies that work by selectively destroying senescent cells are very much in the news of late. One class of senolytic drug candidates works by inducing apoptosis, a form of programmed cell death, via reduced levels of Bcl-2 family proteins, such as Bcl-2 itself, Bcl-xL, and Bcl-W, all of which normally act to suppress apoptosis. Senescent cells are inclined towards apoptosis already, so a modest nudge in that direction can destroy a fair proportion of these unwanted cells without causing harm to healthy cells. These apoptosis-related proteins have numerous other roles as well, however, since evolution is very much in favor of reusing the tools to hand. For example, Bcl-xL is also involved in mitochondrial damage protection, the immune response, cellular respiration and DNA repair: quite the portfolio, and all items that are connected to aging in one way or another. I noted an open access paper today that muddies the water considerably on the topic of Bcl-xL, as it shows that more Bcl-xL rather than less (a) reduces incidence of cellular senescence in tissue cultures, (b) extends life in nematode worms, and © is found in human centenarians, but not younger individuals.

Ordinary somatic cells, the vast majority of the cells in the body, become senescent when they reach the Hayflick limit at the end of their replicative life span, or in response to damage, or a toxic local environment, or as a part of the wound healing process. Senescent cells cease dividing, and most either self-destruct or are destroyed by the immune system soon afterwards. This behavior has evolved because it suppresses cancer incidence, at least initially, by removing those cells most at risk. Unfortunately not all are destroyed, and those that linger cause harm to surrounding tissues via a potent mix of inflammatory signals known as the senescence-associated secretory phenotype (SASP). Given enough senescence cells, as few as 1% or less of all the cells in an organ, significant dysfunction and inflammation is the result, contributing to the development and progression of age-related disease.

Continue reading “Complicating the Picture for Aging, Cellular Senescence, and Bcl-xL” »