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

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Small, DH (2008) Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression? Trends in Molecular Medicine, 14 (3). pp. 103-108. ISSN 1471-4914 (Unpublished)

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Abstract

Accumulation of b-amyloid protein (Ab) in the brain is a key feature of Alzheimer’s disease (AD). The build-up of aggregated forms of Ab leads to synaptic loss and to cognitive dysfunction. Although the pathways controlling production and aggregation of Ab 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- a and a7 nicotinic acetylcholine receptors (a7 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.

Item Type: Article
Journal or Publication Title: Trends in Molecular Medicine
Page Range: pp. 103-108
ISSN: 1471-4914
Identification Number - DOI: 10.1016/j.molmed.2007.12.006
Additional Information: The definitive version is available at http://www.sciencedirect.com
Date Deposited: 19 Nov 2008 03:57
Last Modified: 18 Nov 2014 03:53
URI: http://eprints.utas.edu.au/id/eprint/7960
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