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Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease

Despite of long-standing evidence that beta-amyloid (Aβ) peptides have detrimental effects on synaptic function, the relationship between Aβ, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Aβ peptides is one of th...

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Detalles Bibliográficos
Autores principales: Bayer, Thomas A., Wirths, Oliver
Formato: Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879032/
https://www.ncbi.nlm.nih.gov/pubmed/20552046
http://dx.doi.org/10.3389/fnagi.2010.00008
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author Bayer, Thomas A.
Wirths, Oliver
author_facet Bayer, Thomas A.
Wirths, Oliver
author_sort Bayer, Thomas A.
collection PubMed
description Despite of long-standing evidence that beta-amyloid (Aβ) peptides have detrimental effects on synaptic function, the relationship between Aβ, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Aβ peptides is one of the key events leading to synaptic and neuronal dysfunction. Many studies have been carried out using transgenic mouse models of Alzheimer's disease (AD) which have been proven to be valuable model systems in modern AD research. The present review discusses the impact of intraneuronal Aβ accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations.
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spelling pubmed-28790322010-06-15 Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease Bayer, Thomas A. Wirths, Oliver Front Aging Neurosci Neuroscience Despite of long-standing evidence that beta-amyloid (Aβ) peptides have detrimental effects on synaptic function, the relationship between Aβ, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Aβ peptides is one of the key events leading to synaptic and neuronal dysfunction. Many studies have been carried out using transgenic mouse models of Alzheimer's disease (AD) which have been proven to be valuable model systems in modern AD research. The present review discusses the impact of intraneuronal Aβ accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations. Frontiers Research Foundation 2010-03-10 /pmc/articles/PMC2879032/ /pubmed/20552046 http://dx.doi.org/10.3389/fnagi.2010.00008 Text en Copyright © 2010 Bayer and Wirths. http://www.frontiersin.org/licenseagreement This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
spellingShingle Neuroscience
Bayer, Thomas A.
Wirths, Oliver
Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title_full Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title_fullStr Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title_full_unstemmed Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title_short Intracellular Accumulation of Amyloid-Beta – A Predictor for Synaptic Dysfunction and Neuron Loss in Alzheimer's Disease
title_sort intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in alzheimer's disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879032/
https://www.ncbi.nlm.nih.gov/pubmed/20552046
http://dx.doi.org/10.3389/fnagi.2010.00008
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