[Back to Issue 10 ToC] [Back to Journal Contents] [Back to Biochemistry (Moscow) Home page]
[View Full Article] [Download Reprint (PDF)]

REVIEW: The Programmed Aging Paradigm: How We Get Old


Giacinto Libertini

Independent Researcher; E-mail: giacinto.libertini@tin.it

Biochemistry (Moscow) Office, Maronovsky Pereulok 26, 119049 Moscow, Russia; fax: (499) 238-2479; E-mail: biochem@naukaran.ru; ozrina@bio.chem.msu.ru

Received April 28, 2014
According to the traditional explanations (“old paradigm”), aging is due to the progressive accumulation of heterogeneous damages that are insufficiently contrasted by natural selection. An opposite interpretation (“new paradigm”) sees aging as selectively advantageous in terms of supra-individual natural selection, and this implies the indispensable existence of genetically controlled specific mechanisms that determine it. The aim of this work is to expound synthetically the progressive alterations that mark the aging by showing how these changes are clearly defined and regulated by genes. The possibility of such a description, based on sound evidence, is an essential element for the plausibility of the new paradigm, and a fundamental argument against the tenability of the old paradigm.
KEY WORDS: aging, phenoptosis, programmed aging paradigm, non-programmed aging paradigm, cell turnover, cell senescence, Alzheimer, ARMD

DOI: 10.1134/S0006297914100034