Alzheimer's disease: synapses gone cold

<p>Abstract</p> <p>Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is prim...

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Main Authors: Hyman Bradley T, Koffie Robert M, Spires-Jones Tara L
Format: Article
Language:English
Published: BMC 2011-08-01
Series:Molecular Neurodegeneration
Subjects:
Online Access:http://www.molecularneurodegeneration.com/content/6/1/63
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spelling doaj-3ee3cbfa09674deb924792a4b199a33b2020-11-24T22:02:59ZengBMCMolecular Neurodegeneration1750-13262011-08-01616310.1186/1750-1326-6-63Alzheimer's disease: synapses gone coldHyman Bradley TKoffie Robert MSpires-Jones Tara L<p>Abstract</p> <p>Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is primarily a disease of synaptic dysfunction. Soluble oligomeric forms of amyloid beta (Aβ), the peptide that aggregates to form senile plaques in the brain of AD patients, have been shown to be toxic to neuronal synapses both <it>in vitro </it>and <it>in vivo</it>. Aβ oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD), electrophysiological correlates of memory formation. Furthermore, oligomeric Aβ has also been shown to induce synapse loss and cognitive impairment in animals. The molecular underpinnings of these observations are now being elucidated, and may provide clear therapeutic targets for effectively treating the disease. Here, we review recent findings concerning AD pathogenesis with a particular focus on how Aβ impacts synapses.</p> http://www.molecularneurodegeneration.com/content/6/1/63Alzheimer's diseaseamyloid-betasynapse losslong-term depressionlong-term potentiationcognitive decline
collection DOAJ
language English
format Article
sources DOAJ
author Hyman Bradley T
Koffie Robert M
Spires-Jones Tara L
spellingShingle Hyman Bradley T
Koffie Robert M
Spires-Jones Tara L
Alzheimer's disease: synapses gone cold
Molecular Neurodegeneration
Alzheimer's disease
amyloid-beta
synapse loss
long-term depression
long-term potentiation
cognitive decline
author_facet Hyman Bradley T
Koffie Robert M
Spires-Jones Tara L
author_sort Hyman Bradley T
title Alzheimer's disease: synapses gone cold
title_short Alzheimer's disease: synapses gone cold
title_full Alzheimer's disease: synapses gone cold
title_fullStr Alzheimer's disease: synapses gone cold
title_full_unstemmed Alzheimer's disease: synapses gone cold
title_sort alzheimer's disease: synapses gone cold
publisher BMC
series Molecular Neurodegeneration
issn 1750-1326
publishDate 2011-08-01
description <p>Abstract</p> <p>Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is primarily a disease of synaptic dysfunction. Soluble oligomeric forms of amyloid beta (Aβ), the peptide that aggregates to form senile plaques in the brain of AD patients, have been shown to be toxic to neuronal synapses both <it>in vitro </it>and <it>in vivo</it>. Aβ oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD), electrophysiological correlates of memory formation. Furthermore, oligomeric Aβ has also been shown to induce synapse loss and cognitive impairment in animals. The molecular underpinnings of these observations are now being elucidated, and may provide clear therapeutic targets for effectively treating the disease. Here, we review recent findings concerning AD pathogenesis with a particular focus on how Aβ impacts synapses.</p>
topic Alzheimer's disease
amyloid-beta
synapse loss
long-term depression
long-term potentiation
cognitive decline
url http://www.molecularneurodegeneration.com/content/6/1/63
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AT koffierobertm alzheimersdiseasesynapsesgonecold
AT spiresjonestaral alzheimersdiseasesynapsesgonecold
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