Despite considerable progress in defining the role of the beta-amyloid protein (Abeta) in the pathogenesis of Alzheimer's disease (AD), the mechanism by which accumulation of Abeta causes dementia remains elusive. Memory loss is probably caused by an Abeta-induced change in synaptic plasticity. Computational neuroscience (neural network modelling) studies demonstrate that cell death (or synaptic loss as a consequence of cell death) per se cannot cause the specific pattern of gradual amnesia that occurs in AD. Amnesia typical of that seen in AD can only be produced when synaptic scaling occurs. Synaptic scaling is a compensatory homeostatic mechanism which maintains the excitatory response of individual neurons and prevents the catastrophic amnesia associated with synapse loss. In this review, several possible mechanisms of synaptic scaling are described.

Item Type:	Refereed Article
Research Division:	Medical and Health Sciences
Research Group:	Neurosciences
Research Field:	Neurosciences not elsewhere classified
Objective Division:	Health
Objective Group:	Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:	Neurodegenerative Disorders Related to Ageing
UTAS Author:	Small, DH (Professor David Small)
ID Code:	63316
Year Published:	2004
Web of Science® Times Cited:	22
Deposited By:	Menzies Institute for Medical Research
Deposited On:	2010-04-28
Last Modified:	2010-09-16
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