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The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease

Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer’s disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropatholo...

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Autores principales: Ziegler-Waldkirch, Stephanie, Meyer-Luehmann, Melanie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297249/
https://www.ncbi.nlm.nih.gov/pubmed/30618627
http://dx.doi.org/10.3389/fncel.2018.00473
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author Ziegler-Waldkirch, Stephanie
Meyer-Luehmann, Melanie
author_facet Ziegler-Waldkirch, Stephanie
Meyer-Luehmann, Melanie
author_sort Ziegler-Waldkirch, Stephanie
collection PubMed
description Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer’s disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropathological hallmarks are amyloid-β (Aβ) plaques and neurofibrillary tangles. In the brain of AD patients and in mouse models of AD several morphological and functional changes, such as microgliosis and astrogliosis around Aβ plaques, as well as dendritic and synaptic alterations, are associated with these lesions. In this review article, we will summarize the current literature on synapse loss in mouse models of AD and discuss current and prospective treatments for AD.
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spelling pubmed-62972492019-01-07 The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease Ziegler-Waldkirch, Stephanie Meyer-Luehmann, Melanie Front Cell Neurosci Neuroscience Synapse loss has detrimental effects on cellular communication, leading to network disruptions within the central nervous system (CNS) such as in Alzheimer’s disease (AD). AD is characterized by a progressive decline of memory function, cognition, neuronal and synapse loss. The two main neuropathological hallmarks are amyloid-β (Aβ) plaques and neurofibrillary tangles. In the brain of AD patients and in mouse models of AD several morphological and functional changes, such as microgliosis and astrogliosis around Aβ plaques, as well as dendritic and synaptic alterations, are associated with these lesions. In this review article, we will summarize the current literature on synapse loss in mouse models of AD and discuss current and prospective treatments for AD. Frontiers Media S.A. 2018-12-11 /pmc/articles/PMC6297249/ /pubmed/30618627 http://dx.doi.org/10.3389/fncel.2018.00473 Text en Copyright © 2018 Ziegler-Waldkirch and Meyer-Luehmann. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Ziegler-Waldkirch, Stephanie
Meyer-Luehmann, Melanie
The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title_full The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title_fullStr The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title_full_unstemmed The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title_short The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer’s Disease
title_sort role of glial cells and synapse loss in mouse models of alzheimer’s disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297249/
https://www.ncbi.nlm.nih.gov/pubmed/30618627
http://dx.doi.org/10.3389/fncel.2018.00473
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