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dc.contributor.authorShankar, Ganesh M
dc.contributor.authorWalsh, Dominic M
dc.date.accessioned2011-11-21T08:47:40Z
dc.date.available2011-11-21T08:47:40Z
dc.date.issued2009-11-23
dc.identifierhttp://dx.doi.org/10.1186/1750-1326-4-48
dc.identifier.citationMolecular Neurodegeneration. 2009 Nov 23;4(1):48
dc.identifier.urihttp://hdl.handle.net/10147/190070
dc.description.abstractAbstract Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. Accordingly, it has been proposed that synapse loss underlies the memory impairment evident in the early phase of AD and that since plasticity is important for neuronal viability, persistent disruption of plasticity may account for the frank cell loss typical of later phases of the disease. Extensive multi-disciplinary research has implicated the amyloid β-protein (Aβ) in the aetiology of AD and here we review the evidence that non-fibrillar soluble forms of Aβ are mediators of synaptic compromise. We also discuss the possible mechanisms of Aβ synaptotoxicity and potential targets for therapeutic intervention.
dc.titleAlzheimer's disease: synaptic dysfunction and Abeta
dc.typeJournal Article
dc.language.rfc3066en
dc.rights.holderShankar et al.; licensee BioMed Central Ltd.
dc.description.statusPeer Reviewed
dc.date.updated2011-11-18T20:05:28Z
refterms.dateFOA2018-08-22T15:00:57Z
html.description.abstractAbstract Synapse loss is an early and invariant feature of Alzheimer's disease (AD) and there is a strong correlation between the extent of synapse loss and the severity of dementia. Accordingly, it has been proposed that synapse loss underlies the memory impairment evident in the early phase of AD and that since plasticity is important for neuronal viability, persistent disruption of plasticity may account for the frank cell loss typical of later phases of the disease. Extensive multi-disciplinary research has implicated the amyloid β-protein (Aβ) in the aetiology of AD and here we review the evidence that non-fibrillar soluble forms of Aβ are mediators of synaptic compromise. We also discuss the possible mechanisms of Aβ synaptotoxicity and potential targets for therapeutic intervention.


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