Abstract
There is ample support for the hypothesis that free radical molecules play a major role in aging (Harman, 1981; Pryor, 1984; Packer, 1984; Cutler, 1985). This is also true for the pathological changes associated with aging brain (Agranoff, 1984; Cutler, 1985) although the bulk of studies on free radical processes in the nervous system have focused on acute neural tissue injury (Demopoulos et al., 1979; Naftchi and Gennaro, 1985; Willmore et al., 1983; Chan et al., 1984; Anderson and Means, 1985; Anderson et al., 1985). Although the relative contributions of the different components of auto-oxidation events are not fully resolved at the chemical level [see Aust et al. (1985) and Halliwell and Gutteridge (1985) for two views], there is little doubt that lipid peroxidation events, irrespective of the sources of catalysis, and endogenous levels of “scavenging enzymes” are predictive of pathological consequences. Given the cellular heterogeneity and level of intercellular communication peculiar to the nervous system, there are advantages to the development and use of an in vitro system where pertinent variables can be controlled.
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© 1987 Martinus Nijhoff Publishing, Boston
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Perez-Polo, R., Werrbach-Perez, K. (1987). In Vitro Model of Neuronal Aging and Development in the Nervous System. In: Vernadakis, A., Privat, A., Lauder, J.M., Timiras, P.S., Giacobini, E. (eds) Model Systems of Development and Aging of the Nervous System. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2037-1_28
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DOI: https://doi.org/10.1007/978-1-4613-2037-1_28
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