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Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits
Alzheimer’s disease (AD) is a neurodegenerative disease that is characterized by the production and deposition of β-amyloid protein (Aβ) and hyperphosphorylated tau, leading to the formation of β-amyloid plaques (APs) and neurofibrillary tangles (NFTs). Although calcium ions (Ca(2+)) promote the for...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674839/ https://www.ncbi.nlm.nih.gov/pubmed/34924952 http://dx.doi.org/10.3389/fnmol.2021.757515 |
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author | Guan, Pei-Pei Cao, Long-Long Yang, Yi Wang, Pu |
author_facet | Guan, Pei-Pei Cao, Long-Long Yang, Yi Wang, Pu |
author_sort | Guan, Pei-Pei |
collection | PubMed |
description | Alzheimer’s disease (AD) is a neurodegenerative disease that is characterized by the production and deposition of β-amyloid protein (Aβ) and hyperphosphorylated tau, leading to the formation of β-amyloid plaques (APs) and neurofibrillary tangles (NFTs). Although calcium ions (Ca(2+)) promote the formation of APs and NFTs, no systematic review of the mechanisms by which Ca(2+) affects the development and progression of AD has been published. Therefore, the current review aimed to fill the gaps between elevated Ca(2+) levels and the pathogenesis of AD. Specifically, we mainly focus on the molecular mechanisms by which Ca(2+) affects the neuronal networks of neuroinflammation, neuronal injury, neurogenesis, neurotoxicity, neuroprotection, and autophagy. Furthermore, the roles of Ca(2+) transporters located in the cell membrane, endoplasmic reticulum (ER), mitochondria and lysosome in mediating the effects of Ca(2+) on activating neuronal networks that ultimately contribute to the development and progression of AD are discussed. Finally, the drug candidates derived from herbs used as food or seasoning in Chinese daily life are summarized to provide a theoretical basis for improving the clinical treatment of AD. |
format | Online Article Text |
id | pubmed-8674839 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86748392021-12-17 Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits Guan, Pei-Pei Cao, Long-Long Yang, Yi Wang, Pu Front Mol Neurosci Molecular Neuroscience Alzheimer’s disease (AD) is a neurodegenerative disease that is characterized by the production and deposition of β-amyloid protein (Aβ) and hyperphosphorylated tau, leading to the formation of β-amyloid plaques (APs) and neurofibrillary tangles (NFTs). Although calcium ions (Ca(2+)) promote the formation of APs and NFTs, no systematic review of the mechanisms by which Ca(2+) affects the development and progression of AD has been published. Therefore, the current review aimed to fill the gaps between elevated Ca(2+) levels and the pathogenesis of AD. Specifically, we mainly focus on the molecular mechanisms by which Ca(2+) affects the neuronal networks of neuroinflammation, neuronal injury, neurogenesis, neurotoxicity, neuroprotection, and autophagy. Furthermore, the roles of Ca(2+) transporters located in the cell membrane, endoplasmic reticulum (ER), mitochondria and lysosome in mediating the effects of Ca(2+) on activating neuronal networks that ultimately contribute to the development and progression of AD are discussed. Finally, the drug candidates derived from herbs used as food or seasoning in Chinese daily life are summarized to provide a theoretical basis for improving the clinical treatment of AD. Frontiers Media S.A. 2021-12-02 /pmc/articles/PMC8674839/ /pubmed/34924952 http://dx.doi.org/10.3389/fnmol.2021.757515 Text en Copyright © 2021 Guan, Cao, Yang and Wang. https://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 | Molecular Neuroscience Guan, Pei-Pei Cao, Long-Long Yang, Yi Wang, Pu Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title | Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title_full | Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title_fullStr | Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title_full_unstemmed | Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title_short | Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits |
title_sort | calcium ions aggravate alzheimer’s disease through the aberrant activation of neuronal networks, leading to synaptic and cognitive deficits |
topic | Molecular Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674839/ https://www.ncbi.nlm.nih.gov/pubmed/34924952 http://dx.doi.org/10.3389/fnmol.2021.757515 |
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