Abstract
Alzheimer’s disease (AD) has been linked to deficits in several neurotransmitter and neuropeptide systems. Deficits in central noradrenergic, serotonergic, dopaminergic, and somatostatinergic systems have been reported (for review see Rossor and Iversen, 1986). The most consistent degeneration, however, involves the cholinergic system. Biochemical studies of brain specimens from patients with a clinical diagnosis of AD demonstrate large reductions in cholinergic markers such as choline uptake, choline acetyltransferase activity, acetylcholine synthesis, acetylcholine release and number of nicotinic receptors (for review see Adem, 1987). These studies suggest that at least some symptoms of AD are related to the cholinergic deficit and might be ameliorated by manipulations of cholinergic neurotransmission. Pharmacological strategies aimed at increasing cholinergic neurotransmission may attempt to stimulate cholinergic receptors, increase release or synthesis of acetylcholine, or delay of its synaptic degradation. Studies in which delay in acetylcholine degradation was sought focused on physostigmine and tetrahydroaminoacridine (THA).
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Winblad, B., Adem, A., Backman, L., Nordberg, A., Elinder, F., Arhem, P. (1991). Cholinesterase Inhibitors in Alzheimer’s Disease: Evaluation of Clinical Studies. In: Becker, R., Giacobini, E. (eds) Cholinergic Basis for Alzheimer Therapy. Advances in Alzheimer Disease Therapy. Birkhäuser, Boston, MA. https://doi.org/10.1007/978-1-4899-6738-1_28
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DOI: https://doi.org/10.1007/978-1-4899-6738-1_28
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