Now is a great time to donate and help to unlock the stretch goals.
https://www.lifespan.io/mitomouse
Longecity is also offering ways to match your donations and you can find out more about that on the project page.
Category: life extension – Page 376
Talks at Google
Posted in biological, genetics, life extension
David Sinclair, professor of genetics at Harvard Medical School, discusses his new book “Lifespan”, which distills his cutting-edge research findings on the biological processes underpinning aging. Sinclair describes lifestyle hacks we can undertake now to combat aging, as well as future scientific breakthroughs that promise to slow down—and even reverse—the aging process.
Moderated by: Sam Phippen
Get the book: https://goo.gle/2LXCd2P
Second prize is a trip to meet Dr. Aubrey de Grey! This international (short) film competition is presented by the SENS Research Foundation, the International Longevity Alliance and Heales. The winning film will be chosen by our remarkable jury. For more information on how to compete and to sign up please visit www.longevityfilmcompetition.com
Click on photo to start video.
I just arrived home in L.A. from RAADfest in Las Vegas. What a WONDERFUL event! For the 4th consecutive year I had the opportunity to sing, (this time kicking off the event), speak and moderate. But the most important part was to be among such incredible human beings. I feel so grateful to be part of a community of brilliant minds, passionate and visionary people, who work so hard to stop the suffering of the ill health, isolation, horror and death that aging brings to us. The video has short bites of the soundcheck for my song and the ending live. A professionally done video with the complete song will be available at some point and I will post it! #RAADfest2019 #RAAD2019 #RAADfest
A team of researchers, including Dr. David Sinclair, has recently made a new study available as a preprint prior to peer review and publication in the journal Cell.
DNA damage and the double-strand break
Two of the primary hallmarks of aging are genomic instability, which consists of damage to our DNA, and epigenetic alterations, which are the changes in gene expression that occur with aging and are harmful to normal cell function.
As the longevity investor’s new fund turns 8 months old this month, we went five for five with Sergey Young.
Circulating levels of white blood cells (WBCs) are one of the 10 variables used to quantify biological age with PhenoAge (https://michaellustgarten.com/2019/09/09/quantifying-biological-age). The reference range for WBCs is 4.5 – 11 *109 cells/L, but within that range, what’s optimal?
Several studies have reported that WBCs greater than 5 are associated with an increased all-cause mortality risk (Ahmadi-Abhari et al. 2013, Samet et al. 2005, Weijenberg et al. 1996). While observational studies are important for identifying associations with mortality risk, stronger evidence is obtained when the data from the same subjects are tracked for a time period. Perhaps the best evidence for the association between WBCs with mortality risk comes from the Baltimore Longitudinal Study on Aging (BLSA), which studied 2803 men and women over a period of 44 years (Ruggiero et al. 2007). As shown below, subjects that had circulating WBCs between 3.5 – 6 had the best survival, whereas WBCs below 3.5, between 6 – 10, and 10+ each had successively higher risk. The 0.5 point on the y-axis of the curve (survival) is defined as 50% mortality, and is the point where half of the study subjects died, whereas the remaining 50% were still alive.
Do you really want to live forever?
My mission is to drastically improve your life by helping you break bad habits, build and keep new healthy habits to make you the best version of yourself. I read the books and do all the research and share my findings with you!
This video is “Day 0” of RAADFest 2019 in Las Vegas. I discuss various topics and will do my best at RAADFest to interview longevity experts like Bill Faloon, James Strole, Bernadeane, Liz Parrish, Dr. Aubrey de Grey, Dr. Bill Andrews, Dr. Ed Park, Dr. Duncan Ross, Ben Goertzel and hopefully many more. I’ll bring you all the major updates from RAADFest!
Aim: Aging in humans is associated with a 10–40-fold greater incidence of sudden cardiac death from malignant tachyarrhythmia. We have reported that thiol oxidation of ryanodine receptors (RyR2s) by mitochondria-derived reactive oxygen species (mito-ROS) contributes to defective Ca2+ homeostasis in cardiomyocytes (CMs) from aging rabbit hearts. However, mechanisms responsible for the increase in mito-ROS in the aging heart remain poorly understood. Here we test the hypothesis that age-associated decrease in autophagy is a major contributor to enhanced mito-ROS production and thereby pro-arrhythmic disturbances in Ca2+ homeostasis.
Methods and Results: Ventricular tissues from aged rabbits displayed significant downregulation of proteins involved in mitochondrial autophagy compared with tissues from young controls. Blocking autophagy with chloroquine increased total ROS production in primary rabbit CMs and mito-ROS production in HL-1 CMs. Furthermore, chloroquine treatment of HL-1 cells depolarized mitochondrial membrane potential (Δψm) to 50% that of controls. Blocking autophagy significantly increased oxidation of RyR2, resulting in enhanced propensity to pro-arrhythmic spontaneous Ca2+ release under β-adrenergic stimulation. Aberrant Ca2+ release was abolished by treatment with the mito-ROS scavenger mito-TEMPO. Importantly, the autophagy enhancer Torin1 and ATG7 overexpression reduced the rate of mito-ROS production and restored both Δψm and defective Ca2+ handling in CMs derived from aged rabbit hearts.
Conclusion: Decreased autophagy is a major cause of increased mito-ROS production in the aging heart. Our data suggest that promoting autophagy may reduce pathologic mito-ROS during normal aging and reduce pro-arrhythmic spontaneous Ca2+ release via oxidized RyR2s.
The MitoSENS Webinar
Posted in biotech/medical, life extension
Back in January, we were joined by Dr. Aubrey de Grey, Dr. Amutha Boominathan, Dr. Matthew O’Conner, and Michael Rae from the SENS Research Foundation for a webinar discussion panel focused on MitoSENS, the mitochondrial repair program. During the webinar, a number of points were discussed, and the Lifespan Heroes in the audience got to ask the researchers questions about MitoSENS and about the work of the SENS Foundation in general.
In 2015, the MitoSENS team raised funding on Lifespan.io to launch a study testing if they could create mitochondrial DNA copies in the cell nucleus, and they were successful in doing so as a result of the funds they received. In October 2019, the MitoSENS team launched a new follow-up project called MitoMouse, which aims to bring its mitochondrial repair therapy to mammals as a proof of concept on the road to translation to human use.