Lifeboat Foundation

Unlike the rigid skeletons within our bodies, the skeletons within individual cells—cytoskeletons—are changeable, even fluid. And when these cytoskeletons reorganize themselves, they do more than support different cell shapes. They permit different functions.

Little wonder, then, that scientists who build artificial cells hope to create synthetic cytoskeletons that act like natural cytoskeletons. Synthetic cytoskeletons capable of supporting dynamic changes in cell shape and function could enable the development of novel drug delivery systems, diagnostic tools, and regenerative medicine applications.

Synthetic cytoskeletons have incorporated building blocks such as polymers, small molecules, carbon nanotubes, peptides, and DNA nanofilaments. Mostly DNA nanofilaments. Although they offer programmability, they can be hard to fine tune. To get around this difficulty, scientists based at UNC Chapel Hill led by Ronit Freeman, PhD, investigated the relatively unexplored possibilities offered by peptides. Specifically, the scientists engineered artificial cells using a programmable peptide–DNA nanotechnology approach.

Thsi is a year old. But at 27 minutes David gets asked a couple fo “when” questions.

Dr. David Sinclair presents the progress of epigenetic reprogramming and rejuvenation in this video. He’s also answering questions on when he thinks the rejuvenation therapy be available in the Q\&A session at the end of the presentation.

Continue reading “Will Rejuvenation Therapy Be Available In Our LIFETIME? Gene Therapy VS Small Molecules” »

Venki Ramakrishnan’s is the real-deal ‘pivot story’ — ‘pivoting’ being quite the fancy thing to do today. Born in Chidambaram in Tamil Nadu in 1952, Venki wanted to be a physicist, and by the time he decided to do something about his passion for Biology, he was already a PhD in Physics from Ohio University, USA. He then ‘pivoted’ and studied Biology at the University of California, San Diego, before he began his post-doctoral work at Yale University.

He went on to win the Nobel Prize in Chemistry in 2009 for his work on cellular particles called ribosomes. His first book, Gene Machine, captures this journey with the kind of honesty and self-deprecation one does not expect from an award-winning scientist.

With similar candour, in his second book, he examines recent scientific breakthroughs in longevity and ageing and raises uncomfortable questions about the ethical aspects of the research as well as the biological purpose of death.

I found this on NewsBreak: Activating a gene that slows brain aging and increases lifespan.

I found this on NewsBreak: The Telomere Paradox: Researchers Discover a Twist in How Diet Affects Aging.

New research reveals how cells prevent telomerase from meddling with double-stranded breaks.

#longevity #science

A study from the University of Michigan has shown that traumatic experiences during childhood may get “under the skin” later in life, impairing the muscle function of people as they age.

The study examined the function of skeletal muscle of older adults paired with surveys of adverse events they had experienced in childhood. It found that people who experienced greater childhood adversity, reporting one or more adverse events, had poorer muscle metabolism later in life. The research, led by University of Michigan Institute for Social Research scientist Kate Duchowny, is published in Science Advances.

Duchowny and her co-authors used muscle tissue samples from people participating in the Study of Muscle, Mobility and Aging, or SOMMA. The study includes 879 participants over age 70 who donated muscle and fat samples as well as other biospecimens. The participants also were given a variety of questionnaires and physical and cognitive assessments, among other tests.

What’s the optimal way to dose a longevity drug like rapamycin? Nils Osmar looks at some different studies that provide a possible answer:

It’s worth noting that mTORC2 is not directly inhibited by rapamycin under most circumstances, but can be under some. Some studies have found that after prolonged use, rapamycin can also begin inhibiting mTORC2 (see study: Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system).

So taking breaks from rapamycin may also be beneficial.

Continue reading “Rapamycin and Longevity: A Few Thoughts On Dosing” »