Aging mechanism as the "down side" of adaptation: a network approach.
Many diverse hypotheses on aging are in play. All from "aging genes" over decreasing telomere length to increased level of gene mutations has been suggested to determine an organism's lifespan, but no unifying theory exists. As part of a growing interest toward more integrative approaches in the field we propose a simplistic model based on the "use-it-or-lose-it" concept: we hypothesize that biological aging is a systemic property and the down side of adaptation in complex biological networks at various levels of organization: from brain over the immune system to specialized tissues or organs. The simple dynamical model undergoes three phases during its lifetime: (1) general plasticity (childhood), (2) optimization/adaptation to given conditions (youth and adolescence) and (3) steady state associated with high rigidity (aging). Furthermore, our model mimics recent data on the dynamics of the immune system during aging and, although simplistic, thus captures essential characteristics of the aging process. Finally, we discuss the abstract model in relation to current knowledge on aging and propose experimental setups for testing some of the theoretical predictions.
Borup
Mia T
MT
Center for Models of Life, The Niels Bohr Institute, Copenhagen, Denmark. borup@nbi.dk <borup@nbi.dk>
Trusina
Ala
A
Andersson
Anna M C
AM
D000222:Adaptation, Physiological / Q000502:physiology*; D000375:Aging / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D000818:Animals; D005075:Biological Evolution; D031204:Caloric Restriction; D016922:Cellular Senescence / Q000502:physiology; D004777:Environment; D008954:Models, Biological; D013601:T-Lymphocytes / Q000502:physiology