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Category: life extension – Page 273

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.

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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.

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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 . 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 —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 cells can continue to multiply and form tumors.

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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 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.

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“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).

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The SENS Research Foundation has apparently already raised four times its annual income thanks to the PulseChain Airdrop.

The PulseChain airdrop supporting aging research

Richard Heart, the founder of HEX, is about to launch a new cryptocurrency called PulseChain. As part of that launch, he has also arranged an airdrop to give away some of the new cryptocurrency in order to support the SENS Research Foundation (SRF).

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We probably at this point should make all animals immortal: 3.

The advance promises to unlock new insights into human biology and disease, aiding in the study of everything from the developing immune system to tissue regeneration to skin cancer.

“Studying biodiversity is not just about exploring the biology of a bunch of interesting organisms, but ultimately for a better understanding of human biology,” developmental biologist and lead study author Hiroshi Kiyonari said via email.

Five years ago, his team began to systematically work out the problem that had so long plagued the opossum field. The first barrier was to collect zygotes (fertilized eggs) at the right time. Ideally, that would be before they began dividing, when they are still a single cell. If you inject CRISPR at this stage, you can be sure all the resulting animals’ cells will carry whatever DNA changes you make. Doing it later can mean some cells but not others will be edited — a less ideal outcome known as mosaicism. Another benefit of collecting fertilized eggs as early as possible is that the shell coat hasn’t had time to thicken.

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The human trial of plasma dilution started in Russia last week. The lead researcher is checking how the biomarkers of aging will change in response to 110% plasma replacement during the therapy, and the difference between the group with albumin addition and without albumin. The trial is open to both Russian citizens and people from other countries. It is a hybrid model where part of the expenditures is paid by the volunteers, and part is provided by the patron of the research. This model allowed to get the trial started in record time — less than 9 months from conception to the start date.

The research group wants to test plasmapheresis in combination with other longevity therapies next to see if plasma dilution prior to the other therapy can enhance the results.

Are you interested in longevity news? Come over to https://youtube.com/x10show for more!

Does blood hold the secret to aging? That’s kind of what an ongoing clinical trial in Russia is trying to find out. Previous experiments carried out in aged mice suggest that plasma dilution has positive effects on cognition and neuroinflammation, and now scientists want to see if the procedure can positively impact humans too.

By the way, don’t forget our conference Ending Age-Related Diseases 2021 is coming soon! Follow this link to learn more and get your ticket:

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