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Neurotransmitters and Second Messengers in Aging and Alzheimer's Disease

1993; Wiley; Volume: 695; Issue: 1 Linguagem: Inglês

10.1111/j.1749-6632.1993.tb23021.x

1749-6632

Paul T. Francis, M‐T. WEBSTER, Iain P. Chessell, Chris Holmes, Gary C. Stratmann, Andrew Procter, A.J. Cross, A. R. Green, David M. Bowen,

Computational Drug Discovery Methods

A substantial loss of cortical cholinergic nerve endings, along with a much more circumscribed cortical degeneration of pyramidal neurons, almost certainly causes glutamatergic hypoactivity in live Alzheimer's patients. These selective pathologies are discussed in terms of therapy. An additional effect of some proposed treatments is emerging as there is evidence that processing pathways for β‐amyloid precursor proteins in cortical pyramidal neurons, a target cell for acetylcholine, are affected by neuronal activity.