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01-03-2010 | Original Paper

Alzheimer’s Disease Amyloid β-Protein and Synaptic Function

Authors: Tomas Ondrejcak, Igor Klyubin, Neng-Wei Hu, Andrew E. Barry, William K. Cullen, Michael J. Rowan

Published in: NeuroMolecular Medicine | Issue 1/2010

Abstract

Alzheimer’s disease (AD) is characterized neuropathologically by the deposition of different forms of amyloid β-protein (Aβ) including variable amounts of soluble species that correlate with severity of dementia. The extent of synaptic loss in the brain provides the best morphological correlate of cognitive impairment in clinical AD. Animal research on the pathophysiology of AD has therefore focussed on how soluble Aβ disrupts synaptic mechanisms in vulnerable brain regions such as the hippocampus. Synapic plasticity in the form of persistent activity-dependent increases or decreases in synaptic strength provide a neurophysiological substrate for hippocampal-dependent learning and memory. Acute treatment with human-derived or chemically prepared soluble Aβ that contains certain oligomeric assemblies, potently and selectively disrupts synaptic plasticity causing inhibition of long-term potentiation (LTP) and enhancement of long-term depression (LTD) of glutamatergic transmission. Over time these and related actions of Aβ have been implicated in reducing synaptic integrity. This review addresses the involvement of neurotransmitter intercellular signaling in mediating or modulating the synaptic plasticity disrupting actions of soluble Aβ, with particular emphasis on the different roles of glutamatergic and cholinergic mechanisms. There is growing evidence to support the view that NMDA and possibly nicotinic receptors are critically involved in mediating the disruptive effect of Aβ and that targeting muscarinic receptors can indirectly modulate Aβ’s actions. Such studies should help inform ongoing and future clinical trials of drugs acting through the glutamatergic and cholinergic systems.

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Title: Alzheimer’s Disease Amyloid β-Protein and Synaptic Function
Authors: Tomas Ondrejcak
Igor Klyubin
Neng-Wei Hu
Andrew E. Barry
William K. Cullen
Michael J. Rowan
Publication date: 01-03-2010
Publisher: Humana Press Inc
Published in: NeuroMolecular Medicine / Issue 1/2010
Print ISSN: 1535-1084
Electronic ISSN: 1559-1174
DOI: https://doi.org/10.1007/s12017-009-8091-0

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Alzheimer’s Disease Amyloid β-Protein and Synaptic Function

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