Preface

Although some review articles have appeared recently (cf. Giacobini’), studies on aging of the cholinergic system have seldom been combined and intergrated in a single volume. Undoubtedly, the present strong interest in the aging process of the cholinergic system has been stimulated by the notion of its major involvement in Alzheimer’s (AD) and in other degenerative diseases leading to dementia. Presently, we need to reach a better understanding of the sequence of degenerative and regenerative processes taking place in choline@ endings during physiological aging. This knowledge will help us to interpret the neuropathological findings and their modification in the course of the disease. One major question remains open: whether or not aging and AD are separated phenomena or whether AD represents an accentuated form of aging. The present special issue addresses several ~ndamental questions related to aging of cholinergic neurons and synapses. The neuromuscular junction, with its relative simplicity, and by lending itself to the combination of multiple methodologies, continues to serve as an excellent model and a major reference point. The classic quartet Smith, Rosenheimer, Fahim and Robbins, with their coauthors, present a remarkable combination of successful approaches directed to analyze the fine effects of denervation and regeneration at the neuromuscular junction. Effects of growth factors, changes in receptors, delayed regeneration and Ca’+ influxes are all examined in great detail. Four papers address similar or related problems in the CNS. The papers of Forster and La1 and Sherman and Friedman address the problem of pharmacological modulation with cholinergic drugs in the aging CNS. Results from aging,and stress induced changes in choline and glutamate are presented by Gilad et al. Zhang et al. analyze the influence of aging on nicotinic receptors. One can perhaps draw an important (and optimistic) conclusion from all these studies. As suggested, one could affirm that “in spite of neuronal degeneration during aging, responses to stress can be maintained by compensatory efforts that remain intact” (Gilad et al.).