Lifeboat Foundation

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PLEASE CLICK ON LINK TO DONATE: http://cryoprize.info 3 Minute video detailing our efforts to make organ transplants safer, less costly and more available to those in need by offering a prize, beginning at $50,000, to the first person or group to successfully freeze, and restore to full function, one of several mammalian organs.

There are approximately 30 trillion cells in a human body and our health is predicated on them properly interacting with and supporting each other, with the immune system playing a particularly pivotal role. One of the defining characteristics of aging is a decline in the proper functioning of our immune system. Centenarians, a rare population of individuals who reach 100 years or more, experience delays in aging-related diseases and mortality which suggests their immune systems remain functional into extreme old age.

Led by researchers from Boston University Chobanian & Avedisian School of Medicine and Tufts Medical Center, a new study finds centenarians harbor distinct immune cell type composition and activity and possess highly functional immune systems that have successfully adapted to a history of sickness allowing for exceptional longevity. These immune cells may help identify important mechanisms to recover from disease and promote longevity.

“Our data support the hypothesis that centenarians have protective factors that enable to recover from disease and reach extreme old ages,” said lead author Tanya Karagiannis, Ph.D., senior bioinformatician, Center for Quantitative Methods and Data Science, Institute for Clinical Research and Health Policy Studies at Tufts Medical Center.

Turning genes on and off as easily and predictably as flicking a switch could be a powerful tool in medicine and biotech. A type of technology called a riboswitch might be the key. The Okinawa Institute of Science and Technology (OIST) in Japan, in collaboration with Astellas Pharma Inc., has developed a new toolkit that uses small molecules to control the activity of a piece of synthetic RNA, and ultimately regulate gene expression. The technology, which was described in the Journal of the American Chemical Society, worked in mammalian cell cultures and in mice.

The ability to precisely control whether a gene is turned on or off is expected to lead to more efficient production of compounds that are made using animal cells, and make gene therapy, cell therapy, and regenerative medicine safer.

For genes to be expressed, cells make many RNA copies of a section of DNA. These RNA copies, called transcripts, are then used to make the protein. This can lead to the introduction of additional genes (either as DNA or RNA) into cells, which can then be used to make new proteins for a wide variety of applications.

“You won’t live forever” is a catchphrase which has often been touted and has so far remained the proven truth of life — of humans and almost every other living being on planet earth. But soon, this catchphrase may well become the truth of the past, as humanity steps forward to attain immortality.

A former Google scientist has made a prediction, which if proven right, may redefine human civilisation as we know it. Ray Kurzweil, whose over 85 per cent of 147 predictions have been proven right, has predicted that humans will become immortal by 2029.

The revelation came when the 75-year-old computer scientist dwelled upon genetics, nanotechnology, robotics and more in a YouTube video posted by channel Adagio.

Advances in antiaging drug/lead discovery in animal models constitute a large body of literature on novel senotherapeutics and geroprotectives. However, with little direct evidence or mechanism of action in humans—these drugs are utilized as nutraceuticals or repurposed supplements without proper testing directions, appropriate biomarkers, or consistent in-vivo models. In this study, we take previously identified drug candidates that have significant evidence of prolonging lifespan and promoting healthy aging in model organisms, and simulate them in human metabolic interactome networks. Screening for drug-likeness, toxicity, and KEGG network correlation scores, we generated a library of 285 safe and bioavailable compounds. We interrogated this library to present computational modeling-derived estimations of a tripartite interaction map of animal geroprotective compounds in the human molecular interactome extracted from longevity, senescence, and dietary restriction-associated genes. Our findings reflect previous studies in aging-associated metabolic disorders, and predict 25 best-connected drug interactors including Resveratrol, EGCG, Metformin, Trichostatin A, Caffeic Acid and Quercetin as direct modulators of lifespan and healthspan-associated pathways. We further clustered these compounds and the functionally enriched subnetworks therewith to identify longevity-exclusive, senescence-exclusive, pseudo-omniregulators and omniregulators within the set of interactome hub genes. Additionally, serum markers for drug-interactions, and interactions with potentially geroprotective gut microbial species distinguish the current study and present a holistic depiction of optimum gut microbial alteration by candidate drugs. These findings provide a systems level model of animal life-extending therapeutics in human systems, and act as precursors for expediting the ongoing global effort to find effective antiaging pharmacological interventions.

Communicated by Ramaswamy H. Sarma.

Advanced age is a shared risk factor for many chronic and debilitating skeletal diseases including osteoporosis and periodontitis. Mesenchymal stem cells develop various aging phenotypes including the onset of senescence, intrinsic loss of regenerative potential and exacerbation of inflammatory microenvironment via secretory factors. This review elaborates on the emerging concepts on the molecular and epigenetic mechanisms of MSC senescence, such as the accumulation of oxidative stress, DNA damage and mitochondrial dysfunction. Senescent MSCs aggravate local inflammation, disrupt bone remodeling and bone-fat balance, thereby contributing to the progression of age-related bone diseases. Various rejuvenation strategies to target senescent MSCs could present a promising paradigm to restore skeletal aging.

Periodic prolonged fasting (PF) extends lifespan in model organisms and ameliorates multiple disease states both clinically and experimentally owing, in part, to its ability to modulate the immune system. However, the relationship between metabolic factors, immunity, and longevity during PF remains poorly characterized especially in humans.

This study aimed to observe the effects of PF in human subjects on the clinical and experimental markers of metabolic and immune health and uncover underlying plasma-borne factors that may be responsible for these effects.

In this rigorously controlled pilot study ( ClinicalTrial.gov identifier, NCT03487679), 20 young males and females participated in a 3D study protocol including assessments of 4 distinct metabolic states: 1) overnight fasted baseline state, 2) 2-h postprandial fed state, 3) 36-h fasted state, and 4 ) final 2-h postprandial re-fed state 12 h after the 36-h fasting period. Clinical and experimental markers of immune and metabolic health were assessed for each state along with comprehensive metabolomic profiling of participant plasma. Bioactive metabolites identified to be upregulated in circulation after 36 h of fasting were then assessed for their ability to mimic the effects of fasting in isolated human macrophage as well as the ability to extend lifespan in Caenorhabditis elegans.

The hNSCs used in the study have been produced and characterised in the Cell Factory and Biobank of Santa Maria Hospital (Terni, Italy), authorised by the Italian Medicine Agency (AIFA) for the production of hNSCs to be used for clinical trials (aM 54/2018). The methodology applied to isolate, expand, characterise and cryopreserve the lines is based on the Neurosphere Assay^26,41,54, and has been used for the production of the cells utilised in phase I trials for Amyotrophic Lateral Sclerosis patients (NCT01640067²³) and for Secondary Progressive Multiple Sclerosis patients (NCT03282760, ongoing).

The entire production process, starting from tissue procurement to cryopreservation is compliant to cGMP guidelines and approved by AIFA. The hNSCs are obtained from foetal brain tissue derived from fetuses that underwent miscarriage or natural in utero death upon receiving the signed informed consent from the mother. Forty-eight hours prior to implantation, hNSCs were plated in the growth medium at a concentration of 10,000 cells/cm². On the day of surgery, hNSCs were collected by centrifugation, viable cells were counted by Trypan blue exclusion criteria, and the correct number of cells were re-suspended in HBSS for the transplant.

SOD1 transgenic male rats were randomly divided into three experimental groups: (i) transplanted with hNSCs (hNSC rats, n = 15); (ii) treated with HBSS (HBSS rats, n = 15) and (iii) untreated (CTRL rats, n = 22). An additional group of non-transgenic littermates (wild-type, WT, n = 9) were used as controls for symptomatic evaluation of the colony. Tacrolimus (FK506) and cyclosporine (cyclosporin A) are the principal immunosuppressive drugs that have been applied for solid organ transplantation^55,56 and have been translated to stem cell treatments for PD⁵⁷ and ALS²². In animal models, despite differences in potency, both drugs showed excellent survival rates for grafts across many comparative studies^58,59. Our previous results^44,45 showed that hNSCs can survive—without signs of rejection—in the rat brain up to 6 months under transient immunosuppression treatment, with cyclosporin A. On the bases of these results, we applied the same immunosuppressive treatment with administration of cyclosporine A (15 mg/kg/day subcutaneous; Sandimmne, Novartis) that was initiated on the day of transplantation and continued for 15 days after surgery (for all animal groups).

Human longevity records may be broken in the next few decades, a new modeling study suggests.