It is true that aging, aging-associated neurological diseases, injury to the CNS, and certain aspects of PNS development are characterized by restriction of growth factor availability to neurons and the resulting neuronal cell death of deprived neurons. This chapter discusses the hypothesis that neuronal cell death is mediated in part by a shift in neuronal oxidant–antioxidant balance and that at least one neuronotrophic factor, nerve growth factor (NGF), regulates cell death by stimulating antioxidant systems. In particular, it is found that NGF does protect neurons in culture from peroxyl radical generators such as 6-hydroxydopamine and hydrogen peroxide, in part, by inducing catalase activity, low levels of which are expressed by neuronal as compared to non-neuronal cell lines. In the rodent brain, there is also preliminary evidence that NGF induces catalase activity. Thus, aging-associated deficits in cholinergic NGF-responsive neurons and the suggested beneficial effects of NGF treatment in CNS may be due to shifts in the oxidant–antioxidant balance as a consequence of changes in NGF activity.
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