Aging Analytics Agency special case study reveals how Switzerland could become the new European Longevity hotspot.
Category: life extension – Page 412
Today, we’re offering another talk from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.
In her talk, Morgan Levine of the Yale School of Medicine discussed epigenetic biomarkers in detail, discussing the ways in which co-methylation networks provide insight into senescent cells and other facets of biological age.
We’re continuing to release talks from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.
Today, we’re releasing a talk from Dr. Doug Ethell, who announced his company’s efforts to combat Alzheimer’s disease, describing where and how this neurodegenerative disease starts and discussing his company’s work on developing therapies for the cribiform plate, which naturally clears amyloid-forming proteins from the brain before they aggregate.
We’re continuing to release talks from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.
In his talk, The Reversal of the Aging of Human Cells: Strategies for Clinical Implementation, Dr. West discussed the differences between germ-line and somatic cells, embryonic regeneration in humans, organisms that do not age, the Weismann Barrier, the ways in which cellular immortality is repressed in human beings (somatic restriction), cellular reprogramming, and how AgeX is attempting to create stem cell populations for regenerative therapies.
“Everyone is searching for a magic pill that will cure ageing,” explains Richard Siow, who heads up ageing research at King’s College London. “The truth is, lifestyle and diet changes are the most realistic way to extend your life. You can’t just adopt these as you get older. You need to start young – we’re ageing from the moment we’re born.”
Of course, diet and exercise alone won’t enable humans to achieve immortality. We profile the scientists and startups trying to hold back time.
Growing evidence supports the antagonistic pleiotropy theory of mammalian aging. Accordingly, changes in gene expression following the pluripotency transition, and subsequent transitions such as the embryonic–fetal transition, while providing tumor suppressive and antiviral survival benefits also result in a loss of regenerative potential leading to age-related fibrosis and degenerative diseases. However, reprogramming somatic cells to pluripotency demonstrates the possibility of restoring telomerase and embryonic regeneration pathways and thus reversing the age-related decline in regenerative capacity. A unified model of aging and loss of regenerative potential is emerging that may ultimately be translated into new therapeutic approaches for establishing induced tissue regeneration and modulation of the embryo-onco phenotype of cancer.
Keywords:
- acetyl-CoA
- aging
- AMPK
- dietary restriction
- DNA methylation
- epigenetics
- mTOR
- pluripotent stem cells
- regeneration
Aging is often defined as a progressive deterioration of an organism over time, wherein the risk of mortality increases exponentially with age in the postreproductive years. Although everyday environmental risks from predation or infectious disease (e.g., stochastic risks) necessarily lead to increased mortality over time, they are not considered core to the definition of the aging process per se [1,2]. Thus, an important criterion of aging is that it encompasses virtually every somatic tissue type, including the gonads (though not necessarily the germ-line cells themselves, given their role in potentially perpetuating the species) [3]. In order to distinguish the aging process from damage that occurs stochastically over time, Benjamin Gompertz described aging as a process leading to an exponential increase in mortality with time, that is, Rm = R0eat where ‘Rm’ represents the probability of mortality between ages ‘t’ and ‘t + 1’.
Researchers at Mayo Clinic have identified the enzyme, called CD38, that is responsible for the decrease in nicotinamide adenine dinucleotide (NAD) during aging, a process that is associated with age-related metabolic decline. Results demonstrated an increase in the presence of CD38 with aging in both mice and humans. The results appear today in Cell Metabolism.
“As we age, we experience a decline in our metabolism and metabolic function. This increases the incidence of age-related metabolic diseases like obesity, diabetes and others,” says Eduardo Chini, M.D., Ph.D., anesthesiologist and researcher for Mayo Clinic’s Robert and Arlene Kogod Center on Aging and lead author of the study. “Previous studies have shown that levels of NAD decline during the aging process in several organisms. This decrease in NAD appears to be, at least in part, responsible for age-related metabolic decline.”
In this study, researchers at the Center on Aging have shown that CD38, an enzyme that is present in inflammatory cells, is directly involved in the process that mediates the age-related NAD decline. Comparing 3- to 32-month-old mice, researchers found that levels of CD38 increased at least two to three times during chronological aging in all tissues tested, including the liver, fat, spleen and skeletal muscle.