Citation

Weiss B. Neurotoxicology 2000; 21(1-2): 67-73.

Affiliation

Department of Environmental Medicine, University of Rochester, School of Medicine and Dentistry, NY 14642, USA. weiss@envmed.rochester.edu

Copyright

(Copyright © 2000, Elsevier Publishing)

DOI

unavailable

PMID

10794386

Abstract

Early development is not the only life stage during which which we see intensified responses to the adverse effects of chemicals. Vulnerability to toxic processes rises again late in life, and in many ways recapitulates the imperfect defenses deployed by the immature organism. One feature common to both early and late phases is a reduced capacity to compensate for impairment. In the first case, the functional mechanisms have yet to evolve. In the second, they have passed into what might be called a post-mature decline. Traced across the life cycle, this progression might be depicted as an inverted U. The developing brain, however, is equipped with immense plastic potential; the aging brain has lost much of its plasticity. The altered function of the aging brain, however, is not simply an outcome of how long the organism has lived. "Aging" is not a mechanistic explanation. Events occurring during life must account for the changes. Older brains are already high-maintenance properties, so that exposure to substances with neurotoxic properties, such as pesticides, may accelerate the process, or exploit its dwindling capacities to resist their effects. From this vantage point, toxicants can act in three ways to depress function during advanced age: they may interfere with brain development, leaving a legacy of diminished redundancy not apparent until it is further compromised during aging; they may hasten the progressive erosion of function observed with certain abilities; they may exert greater effects in the aging brain because the aging nervous system has already undergone a reduction in its ability to withstand toxic challenges.

Language: en