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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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 |
work_keys_str_mv |
AT hymanbradleyt alzheimersdiseasesynapsesgonecold AT koffierobertm alzheimersdiseasesynapsesgonecold AT spiresjonestaral alzheimersdiseasesynapsesgonecold |
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