The search for a fountain of youth has obsessed humankind for millennia, but a new wave of research is showing that the secret may have been running through our veins all along.
Category: life extension – Page 257
Dr. Jennifer Garrison, PhD (http://garrisonlab.com/) is Assistant Professor, Buck Institute for Research on Aging, Founder & Faculty Director, Global Consortium for Reproductive Longevity & Equality (https://www.buckinstitute.org/gcrle/), Assistant Professor in Residence, Cellular and Molecular Pharmacology, UCSF and Adjunct Assistant Professor of Gerontology, USC Leonard Davis School of Gerontology.
Dr. Garrison’s lab is interested in understanding how neuropeptides (a large class of signaling molecules which are secreted from neurons and transmit messages within the brain and across the nervous system) regulate changes in normal and aging animals as well in understanding how they control behavior at both the cell biological and neural circuit level.
Dr. Garrison received her PhD from the University of California San Francisco in Chemistry and Chemical Biology in the laboratory of Dr. Jack Taunton, where she discovered the molecular target of a natural product and elucidated a novel mechanism by which small molecules can regulate protein biogenesis. As a postdoctoral fellow in Dr. Cori Bargmann’s lab at the Rockefeller University, she showed that the nematode C. elegans produces a neuropeptide that is an evolutionary precursor of the mammalian peptides vasopressin and oxytocin, and mapped a neural circuit by which this molecule, nematocin, modulates mating behavior.
Dr. Garrison was named an Alfred P. Sloan Research Fellow and received a Glenn Foundation Award for Research in Biological Mechanisms of Aging in 2,014 and a Next Generation Leader at the Allen Institute for Brain Science in 2015. Her work is funded by the NIH National Institute of General Medical Sciences, the Glenn Foundation for Medical Research, the Alfred P. Sloan Foundation, and the Larry L. Hillblom Foundation.
We interviewed four longevity experts (including several Lifeboat Foundation board members) to learn how they think about their diets. I was particularly struck by how different they all were (except almost all of them fasted)!
Food.
In all our research into longevity so far, from quantifying how we sleep to exploring the science behind whether human life extension is possible, nutrition has remained the most controversial and confusing subject that we’ve covered. For example, when we surveyed 101 of our readers on their longevity diet, we got 101 very different answers. There is little consensus on what the perfect life extension diet should look like.
In case this hasn’t been posted here yet.
Ageing is inevitable, but what if everything we’ve come to believe about ageing is wrong and we’re able to choose our lifespans? What if ageing is a disease?
In this week’s #HealthyLongevity #webinar, Prof David Sinclair from Harvard Medical School shares a bold new theory for why we age. Prof Sinclair is also the author of “Lifespan, Why We Age – and Why We Don’t Have To” (https://lifespanbook.com/).
Register for upcoming webinar sessions at https://nus-sg.zoom.us/webinar/register/9516279955794/WN_JhWMZNz0QGOgNqxtSBYedw.
#NUSMedicine #webinarseries
A DNA robot that can walk across biological cell membranes is the first one that can control living cells’ behaviour. The researchers who made the robot hope that it could improve cell-based precision medicine.
A team led by Hong-Hui Wang and Zhou Nie from Hunan University, China, has created a synthetic molecular robot that walks along the outer membrane of biological cells. The robot, powered by an enzyme’s catalytic activity, traverses across receptors that act as stepping stones on the cell surface. With each step, the robot activates a signal pathway that regulates cell migration. Driven by the robot’s movement, the cells can reach speeds of 24 μm/hour.
The researchers write that the DNA robot offers, for the first time, an opportunity to accurately and predictably control the nanoscale operations that power a live cell. They suggest that similar molecular machines that guide cell behaviours could play a role in cell-based therapies and regenerative medicine.
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Levine’s Biological age calculator is embedded as an Excel file in this link:
Papers referenced in the video:
The baseline levels and risk factors for high-sensitive C-reactive protein in Chinese healthy population.
https://immunityageing.biomedcentral.com/articles/10.1186/s1…0126-7
Commonly used clinical chemistry tests as mortality predictors: Results from two large cohort studies.
https://pubmed.ncbi.nlm.nih.gov/33152050/
All things must die, according to the poet Alfred Lord Tennyson, but that could be about to change.
A growing number of tech billionaires have decided they want to use their enormous wealth to try to help humans “cheat death.”
Amazon’s Jeff Bezos, Alphabet’s Larry Page, Oracle’s Larry Ellison and Palantir’s Peter Thiel are just a few of the super-rich who have taken a keen interest in the fast-emerging field of longevity, according to interviews, books and media reports.
A deepening understanding of the brain has created unprecedented opportunities to alleviate the challenges posed by disability. Scientists and engineers are taking design cues from biology itself to create revolutionary technologies that restore the function of bodies affected by injury, aging, or disease — from prosthetic limbs that effortlessly navigate tricky terrain to digital nervous systems that move the body after a spinal cord injury.
With the establishment of the new K. Lisa Yang Center for Bionics, MIT is pushing forward the development and deployment of enabling technologies that communicate directly with the nervous system to mitigate a broad range of disabilities. The center’s scientists, clinicians, and engineers will work together to create, test, and disseminate bionic technologies that integrate with both the body and mind.
Is an academic doctor and medical technology entrepreneur, working in the field of the computational biology of aging.
Dr. Radenkovic is also a Partner at the SALT Bio-Fund, and a co-founder of Hooke, an elite longevity research clinic in London.
Dr. Radenkovic has a dual degree in medicine and physiology from University College London Medical School, and did her residency at St Thomas’ Hospital in London. She later worked as Research Fellow at King’s College London and at Harvard University.
Dr. Radenkovic has led a variety of projects, including a digital therapeutics company for women and an algorithm for cardiac MRI based on fractal geometry, to major industry acquisitions.
Dr. Radenkovic has over 30 academic papers, 7 grants, and over 40 scientific conference presentations. She is fluent in 5 languages and 3 programming languages.
Red blood cells are the most abundant cell type in blood, carrying oxygen throughout the human body. In blood circulation, they repetitively encounter various levels of oxygen tension. Hypoxia, a low oxygen tension condition, is a very common micro-environmental factor in physiological processes of blood circulation and various pathological processes such as cancer, chronic inflammation, heart attacks and stroke. In addition, an interplay between poor cellular deformability and impaired oxygen delivery is found in various pathological processes such as sickle cell disease. Sickle red blood cells simultaneously undergo drastic mechanical deformation during the sickling and unsickling process.
The interactions between hypoxia and cell biomechanics and the underlying biochemical mechanisms of the accelerated damage in diseased red blood cells are well understood, however, the exact biomechanical consequences of hypoxia contributing to red blood cell degradation (aging) remains elusive.
Researchers from Florida Atlantic University’s College of Engineering and Computer Science, in collaboration with the Massachusetts Institute of Technology (MIT), sought to identify the role of hypoxia on red blood cell aging via the biomechanical pathways. In particular, they examined hypoxia-induced impairment of red blood cell deformability at the single cell level, compared the differences between non-cyclic hypoxia and cyclic hypoxia, and documented any cumulative effect vs. hypoxia cycles, such as aspects that have not been studied quantitatively. Red blood cell deformability is an important biomarker of its functionality.