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Category: life extension – Page 413

Individuals of the same age may not age at the same rate. Quantitative biomarkers of aging are valuable tools to measure physiological age, assess the extent of ‘healthy aging’, and potentially predict health span and life span for an individual. Given the complex nature of the aging process, the biomarkers of aging are multilayered and multifaceted. Here, we review the phenotypic and molecular biomarkers of aging. Identifying and using biomarkers of aging to improve human health, prevent age-associated diseases, and extend healthy life span are now facilitated by the fast-growing capacity of multilevel cross-sectional and longitudinal data acquisition, storage, and analysis, particularly for data related to general human populations. Combined with artificial intelligence and machine learning techniques, reliable panels of biomarkers of aging will have tremendous potential to improve human health in aging societies.

Keywords: physiological age, phenotypic, molecular, age-associated diseases, aging process.

Aging is the time-dependent physiological functional decline that affects most living organisms, which is underpinned by alterations within molecular pathways, and is also the most profound risk factor for many non-communicable diseases. To identify biomarkers of aging would, on one hand, facilitate differentiation of people who are of the same chronological age yet have variant aging rates. Quantitative biomarkers of aging could also define a panel of measurements for ‘healthy aging’ and, even further, predict life span. On the other hand, biomarkers of aging could also assist researchers to narrow their research scope to a specific biological facet in their attempts to explain the biological process behind aging or aging-related diseases. Here, we review the phenotypic and molecular biomarkers of aging. Phenotypic biomarkers can be non-invasive, panoramic, and easy to obtain, whereas molecular biomarkers can reflect some of the molecular mechanisms underlying age status.

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Unfortunately, as we age they begin to breakdown due to damage.

MitoSENS project aims to reverse that damage with the goal of preventing age-related ill health. In their first study, they managed to show that allotopic expression of two mtDNA genes from the nucleus could bring back several functions in a patient cell line.

MitoSENS team is currently running a crowdfunding campaign on Lifespan.io to collect money for the next crucial step of this project. Scientists want to investigate if functional backup copies of mitochondrial DNA genes in the nucleus can replace their mutated counterparts in live animals, and if this could rescue mitochondrial function.

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This year I had the privilege to record in full Liz Parrish talk delivered at RAADfest 2019 (Revolution Against Aging and Death Festival 2019), which took place in Las Vegas, NV from 3 to 6 of October.

During her talk, Liz tells us about recent developments in the field of gene therapy and what her company BioViva is doing to benefit society by harnessing the power of it.

Don’t miss it!!!

https://bioviva-science.com/

Home

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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

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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

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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

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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.

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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.

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