Answering the ultimate question "what is the proximal cause of aging?"

Mikhail V Blagosklonny1

  • 1Department of Cell Stress Biology, Roswell Park Cancer Institute, BLSC, L3-312, Elm and Carlton Streets, Buffalo, NY 14263, USA. blagosklonny@oncotarget.com

Aging
|February 22, 2013
PubMed

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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