I know that this is controversial in the longevity community, but there was overwhelming agreement among the dentists I talked with that mouthwash is excellent for preventing gingivitis (one study found that it was more effective than flossing) and reducing plaque.
Are you working to extend your healthspan and lifespan? Address the most common aging teeth problems with these dentist-approved tricks.
A summary of the sequel trial for a cocktail of drugs that originally turned back epigenetic clocks by 2.5 years. I do wonder what effect plasma filtering has on the thymus if any.
In this video we review the TRIIM study and look at the trial document for TRIIM-X, the extension study that Dr. Fahy is now conducting.
Timing — If you are familiar with the TRIIM Study please use the time links below to jump to TRIIM-X
0:12 : TRIIM Paper Review.
7:11 : TRIIM-X Trial Review.
08:59 : TRIIM vs TRIIM-X
Papers referred to in this video.
Reversal of epigenetic aging and immunosenescent trends in humans Sept 2019
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826138/
Thymus Regeneration, Immunorestoration, and Insulin Mitigation Extension Trial (TRIIM-X)
Good day to you all.
Sirtuins are once again, making headlines. From a longer lifespan, again, through to helping old and dormant hair follicles to grow new hair, and of course a discourse between certain personalities on twitter, they continue to stimulate the interest and promise so much…
So I have decided to follow up my last sirtuins video with this one, Sirtuins revisited.
Here I look at them all from 1 to 7, to see what is being claimed for each one, and then I look at all the ways we can try to bring them all up to optimum so that we can live long, healthy lives, free from the maladies of old age.
I look at lifestyle interventions from exercise, saunas, cold therapies and more, through to diet choices and then finally on to supplements that are available to boost them all further.
So I hope you find it of use and enjoyable, and have a great weekend.
The University of Surrey has built an artificial intelligence (AI) model that identifies chemical compounds that promote healthy aging — paving the way towards pharmaceutical innovations that extend a person’s lifespan.
In a paper published by Nature Communication’s Scientific Reports, a team of chemists from Surrey built a machine learning model based on the information from the DrugAge database to predict whether a compound can extend the life of Caenorhabditis elegans — a translucent worm that shares a similar metabolism to humans. The worm’s shorter lifespan gave the researchers the opportunity to see the impact of the chemical compounds.
The AI singled out three compounds that have an 80 percent chance of increasing the lifespan of elegans:
Bioprinting in seconds.
Biofabrication technologies, including stereolithography and extrusion-based printing, are revolutionizing the creation of complex engineered tissues. The current paradigm in bioprinting relies on the additive layer-by-layer deposition and assembly of repetitive building blocks, typically cell-laden hydrogel fibers or voxels, single cells, or cellular aggregates. The scalability of these additive manufacturing technologies is limited by their printing velocity, as lengthy biofabrication processes impair cell functionality. Overcoming such limitations, the volumetric bioprinting of clinically relevant sized, anatomically shaped constructs, in a time frame ranging from seconds to tens of seconds is described. An optical-tomography-inspired printing approach, based on visible light projection, is developed to generate cell-laden tissue constructs with high viability (85%) from gelatin-based photoresponsive hydrogels. Free-form architectures, difficult to reproduce with conventional printing, are obtained, including anatomically correct trabecular bone models with embedded angiogenic sprouts and meniscal grafts. The latter undergoes maturation in vitro as the bioprinted chondroprogenitor cells synthesize neo-fibrocartilage matrix. Moreover, free-floating structures are generated, as demonstrated by printing functional hydrogel-based ball-and-cage fluidic valves. Volumetric bioprinting permits the creation of geometrically complex, centimeter-scale constructs at an unprecedented printing velocity, opening new avenues for upscaling the production of hydrogel-based constructs and for their application in tissue engineering, regenerative medicine, and soft robotics.
Mitochondrial Quality Control (Mitophagy), CNS Disorders, and Aging — Dr. Spring Behrouz, Ph.D., CEO, Vincere Biosciences Inc. / CEO, Neuroinitiative LLC.
Dr. Bahareh (Spring) Behrouz, PhD, is the CEO of Vincere Biosciences Inc (https://vincerebio.com/), a biotech company focused on developing novel, small molecule therapeutics targeting mitochondrial pathways and the improvement of mitochondrial quality.
Dr. Behrouz is also the CEO of NeuroInitiative, LLC (https://www.neuroinitiative.com/), a computational biology company she co-founded in 2014, which develops simulations of disease using their patented software platform. A core focus of her research at NeuroInitiative is on the elucidation of complex, converging pathways that contribute to the pathogenesis of Parkinson’s disease (PD), a neuro-degenerative brain disorder which dramatically effects movement, which nearly one million people in the U.S. are living with, and 10 million patients worldwide.
Dr. Behrouz received her graduate training at Michigan State University in the laboratory of Dr. John Goudreau and studied differential susceptibility of dopaminergic neuron sub-types in models of PD. She completed her post-doctoral training in the laboratory of Dr. Matthew Farrer at the Mayo Clinic in Jacksonville, where she primarily focused on in-vivo and primary culture models of LRRK2-mediated pathogenesis and was part of the team that discovered a new pathogenic mutation in VPS35.
An aging/longevity/junk dna link.
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The human body is essentially made up of trillions of living cells. It ages as its cells age, which happens when those cells eventually stop replicating and dividing. Scientists have long known that genes influence how cells age and how long humans live, but how that works exactly remains unclear. Findings from a new study led by researchers at Washington State University have solved a small piece of that puzzle, bringing scientists one step closer to solving the mystery of aging.
A research team headed by Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of cells. The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).
The telomerase gene controls the activity of the telomerase enzyme, which helps produce telomeres, the caps at the end of each strand of DNA that protect the chromosomes within our cells. In normal cells, the length of telomeres gets a little bit shorter every time cells duplicate their DNA before they divide. When telomeres get too short, cells can no longer reproduce, causing them to age and die. However, in certain cell types—including reproductive cells and cancer cells —the activity of the telomerase gene ensures that telomeres are reset to the same length when DNA is copied. This is essentially what restarts the aging clock in new offspring but is also the reason why cancer cells can continue to multiply and form tumors.
Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.
In a study published today in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain — ‘scaffolding’ around nerve cells—lead to loss of memory with aging, but that it is possible to reverse these using genetic treatments.
Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity—the ability of the brain to learn and adapt—and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimized. Then, plasticity is partially turned off, making the brain more efficient but less plastic.
“What is exciting about this is that although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents,” says Fawcett. “This suggests that it may be possible to prevent humans from developing memory loss in old age.”
An intriguing new study from researchers in the United Kingdom is proposing an innovative method to treat age-related memory loss. The preclinical research shows memory decline in aging mice can be reversed by manipulating the composition of structures in the brain known as perineuronal nets.
Perineuronal nets (PNNs) are structures in the brain that envelop certain subsets of neurons, helping stabilize synaptic activity. They essentially put the brakes on the neuroplasticity seen in the first few years of life.
Although PNNs are vital to the effective functioning of a mature adult brain, by their very nature they also limit future neural plasticity and adaptability. A new wave of research is beginning to investigate ways to modulate PNNs in adult brains in the hope of treating a variety of diseases from diabetes to post-traumatic stress disorder (PTSD).
The University of Surrey has built an artificial intelligence (AI) model that identifies chemical compounds that promote healthy aging—paving the way towards pharmaceutical innovations that extend a person’s lifespan.
