A Novel Theory of Aging — Independent of Damage Accumulation

08-09-2023

“We argue that in multicellular organisms, neighbouring cells are in constant competition.”

Listen to an audio version of this press release

BUFFALO, NY- August 9, 2023 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 14, entitled, “A novel theory of ageing independent of damage accumulation.”

The underlying cause or causes of aging are an enduring mystery, but in 1977 Kirkwood postulated that organisms might gain a fitness advantage by reducing investment in somatic maintenance if this allowed them to invest more resources in more crucial processes such as reproduction. The accumulation of somatic damage was therefore inevitable, and his disposable soma theory has dominated gerontology ever since. 

However, as our understanding of aging increases, it is becoming increasingly difficult to align all the aspects of aging with accumulating damage. For example, mutations that increase damage accumulation can also increase longevity, while rejuvenation revelations such as parabiosis and Yamanaka factors indicate that youthfulness can be regained without high energetic cost and despite high levels of damage. 

In their new editorial, researchers James Wordsworth and Daryl Shanley from Newcastle University discuss their recently published paper on selective destruction theory (SDT). SDT suggests a mechanism of aging which is both independent of accumulating damage and consistent with epigenetic rejuvenation. The authors use agent-based modeling to describe how aging could undergo positive selection independent of energetic costs.

“The mechanism of selective destruction is currently theoretical. In our most developed model, we demonstrated that if slow cells induced epigenetic changes in faster cells causing their metabolism to slow (rather than killing them) it not only reduced unnecessary cell death, but also further reduced the likelihood of overactivity disorders by preventing the spread of fast cells.”

Continue reading: DOI: https://doi.org/10.18632/aging.204956 

Corresponding Author: James Wordsworth

Corresponding Email: James.Wordsworth2@newcastle.ac.uk 

Keywords: ageing, evolution, damage, cell competition, metabolic slowdown

Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.https://doi.org/10.18632/aging.204956

About Aging-US:

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

Please visit our website at www.Aging-US.com and connect with us:

For media inquiries, please contact media@impactjournals.com.