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Mechanisms of synaptic homeostasis in Alzheimer's disease
Citation
Small, DH, Mechanisms of synaptic homeostasis in Alzheimer's disease, Current Alzheimer Research, 1, (1) pp. 27-32. ISSN 1567-2050 (2004) [Refereed Article]
DOI: doi:10.2174/1567205043480573
Abstract
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 Details
Item Type: | Refereed Article |
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Research Division: | Biomedical and Clinical Sciences |
Research Group: | Neurosciences |
Research Field: | Neurosciences not elsewhere classified |
Objective Division: | Health |
Objective Group: | Clinical health |
Objective Field: | Clinical health not elsewhere classified |
UTAS Author: | Small, DH (Professor David Small) |
ID Code: | 63316 |
Year Published: | 2004 |
Web of Science® Times Cited: | 27 |
Deposited By: | Menzies Institute for Medical Research |
Deposited On: | 2010-04-28 |
Last Modified: | 2010-09-16 |
Downloads: | 0 |
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