Alzheimer's Disease: Synaptic Dysfunction and Aβ

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Alzheimer's Disease: Synaptic Dysfunction and Aβ

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Title: Alzheimer's Disease: Synaptic Dysfunction and Aβ
Author: Shankar, Ganesh Mani; Walsh, Dominic M.

Note: Order does not necessarily reflect citation order of authors.

Citation: Shankar, Ganesh M., and Dominic M. Walsh. 2009. Alzheimer's disease: synaptic dysfunction and Aβ. Molecular Neurodegeneration 4: 48.
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Abstract: 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.
Published Version: doi://10.1186/1750-1326-4-48
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788538/pdf/
http://www.tbiomed.com/content/4/1/4
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:4817375

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