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Surveying Low-Cost Methods to Measure Lifespan and Healthspan in Caenorhabditis elegans
Published on: May 18, 2022
Answering the ultimate question "what is the proximal cause of aging?"
1Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3-312, Elm and Carlton Streets, Buffalo, NY 14263, USA. blagosklonny@oncotarget.com
Abstract:
Recent discoveries suggest that aging is neither driven by accumulation of molecular damage of any cause, nor by random damage of any kind. Some predictions of a new theory, quasi-programmed hyperfunction, have already been confirmed and a clinically-available drug slows aging and delays diseases in animals. The relationship between diseases and aging becomes easily apparent. Yet, the essence of aging turns out to be so startling that the theory cannot be instantly accepted and any possible arguments are raised for its disposal. I discuss that these arguments actually support a new theory. Are any questions remaining? And might accumulation of molecular damage still play a peculiar role in aging?
Insights
Aging may not stem from accumulated damage but from a quasi-programmed hyperfunction. This theory, supported by drug trials in animals, challenges conventional aging research and suggests a new understanding of age-related diseases.
Area of Science:
- Gerontology
- Molecular Biology
- Biomedical Science
Background:
- Conventional theories posit aging results from accumulated molecular damage.
- Emerging research challenges this, suggesting alternative aging drivers.
- The link between aging and age-related diseases is well-established.
Purpose of the Study:
- To present and support the quasi-programmed hyperfunction theory of aging.
- To address arguments against this new theory.
- To explore the potential role of molecular damage in aging.
Main Methods:
- Review and synthesis of recent aging research findings.
- Analysis of predictions from the quasi-programmed hyperfunction theory.
- Discussion of counterarguments and their implications for the theory.
Main Results:
- Some predictions of the quasi-programmed hyperfunction theory have been experimentally confirmed.
- A clinically available drug has demonstrated efficacy in slowing aging and delaying diseases in animal models.
- Arguments against the theory were found to indirectly support it.
Conclusions:
- The quasi-programmed hyperfunction theory offers a novel framework for understanding aging.
- The theory's implications for age-related diseases warrant further investigation.
- The precise role of molecular damage in this new aging paradigm requires continued study.
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