#260
Totally agree.
Unless ones idea of living forever is in the realm of preserving ones memories, experiences, emotions through some form of mind uploading + the technology to replay the upload (none of which is yet possible), physical immortality of oneself sounds plain crazy. On the other hand who wouldn’t want to stay as healthy and rejuvenated as possible and avoid succumbing to age-related diseases like cancer, arthritis, and dementia? Not too many I think.
https://medium.com/@yurideigin/reversing-aging-epigenetic-rejuvenation-8c498103c353

Scientists have known for a long time that Nature has the power to rejuvenate cells — after all, every new baby is born young despite having started as an oocyte of the same age as its mother (all human oocytes are formed while the mother herself is an embryo).
However, only about a decade ago have we managed to harness that power for ourselves. In 2006 Yamanaka and Takahashi have discovered that using 4 DNA transcription factors (Oct4, Sox2, Klf4 and c‐Myc, abbreviated as OSKM) an adult cell can be turned back into an essentially embryonic stem cell. Of course, in hindsight, early signs that this is possible can be traced as far back as 1962 when Sir John B. Gurdon has shown that he could clone a frog using the nucleus harvested from its adult cell. Both Gurdon and Yamanaka received a Nobel Prize in 2012 for their groundbreaking insights.
Reprogramming, currently an experimental tool to study development and cellular differentiation, may provide additional insights into the mechanisms of aging. Proposed drivers of physiological aging include the accumulation of DNA damage, increased ROS production, telomere shortening, cellular senescence, and defects in nuclear envelope architecture (Bernardes de Jesus and Blasco, 2013; Guarente, 2008;Haigis and Sinclair, 2009; Kennedy and Lamming, 2016; Soultoukis and Partridge, 2016; Steffen and Dillin, 2016). Multiple studies using animal models have demonstrated that the manipulation of these aging drivers leads to the manifestation of molecular hallmarks of aging that are shared between premature aging models and physiological aging (Garcia-Prat et al., 2016; Mitchell et al., 2015). We hypothesize that the emergence of these molecular hallmarks during organismal aging results from the translation of aging signals by a unique and universal epigenetic program. Our results suggest that this epigenetic program, which is reset during embryogenesis, can also be experimentally altered by partial cellular reprogramming at later stages of life. Resetting of the aging clock by epigenetic reprogramming, which is also observed during somatic nuclear transfer, might allow for a deeper understanding of the molecular and cellular mechanisms underlying the aging process. Eventually, it may, as well, lead to the development of therapeutic strategies with the goal of ameliorating age-related diseases and thus improving health and longevity.

Posted by: krypton | Jul 5 2020 22:04 utc | 302