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Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?

Citation

Small, DH, Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?, Trends in Molecular Medicine, 14, (3) pp. 103-108. (2008) [Substantial Review]

DOI: doi:10.1016/j.molmed.2007.12.006

Abstract

Accumulation of β-amyloid protein (Aβ) in the brain is a key feature of Alzheimer's disease (AD). The build-up of aggregated forms of Aβ leads to synaptic loss and to cognitive dysfunction. Although the pathways controlling production and aggregation of Aβ are well studied, the mechanisms that drive the spread of neurodegeneration in the brain are unclear. Here, the idea is presented that AD progresses as a consequence of synaptic scaling, a type of neuronal plasticity that helps maintain synaptic signal strength. Recent studies indicate that brain-derived neurotrophic factor, tumour necrosis factor-α and α7 nicotinic acetylcholine receptors (α7 nAChRs) regulate synaptic scaling in the AD brain. It is suggested that further studies on synaptic scaling in AD could reveal new targets for therapeutic drug development. © 2008 Elsevier Ltd. All rights reserved.

Item Details

Item Type:Substantial Review
Research Division:Biological Sciences
Research Group:Biochemistry and Cell Biology
Research Field:Cell Neurochemistry
Objective Division:Health
Objective Group:Specific Population Health (excl. Indigenous Health)
Objective Field:Health Related to Ageing
UTAS Author:Small, DH (Professor David Small)
ID Code:53136
Year Published:2008
Web of Science® Times Cited:60
Deposited By:Menzies Institute for Medical Research
Deposited On:2008-11-03
Last Modified:2009-04-27
Downloads:0

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