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Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence

Alzheimer’s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated t...

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Autores principales: Khezri, Mohammad Rafi, Mohebalizadeh, Mehdi, Ghasemnejad-Berenji, Morteza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10012555/
https://www.ncbi.nlm.nih.gov/pubmed/36918870
http://dx.doi.org/10.1186/s12964-023-01072-w
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author Khezri, Mohammad Rafi
Mohebalizadeh, Mehdi
Ghasemnejad-Berenji, Morteza
author_facet Khezri, Mohammad Rafi
Mohebalizadeh, Mehdi
Ghasemnejad-Berenji, Morteza
author_sort Khezri, Mohammad Rafi
collection PubMed
description Alzheimer’s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated tau proteins. Increasing evidence suggest that targeting the process of Aβ production to reduce its deposition can serve as a therapeutic option for AD management. In this regard, therapeutic interventions shown that a disintegrin and metalloproteinase domain-containing protein (ADAM) 10, involved in non-amyloidogenic pathway of amyloid precursor protein processing, is known to be a suitable candidate. Therefore, this review aims to examine the molecular properties of ADAM10, its role in AD, and introduce it as a therapeutic target to reduce the progression of the disease. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01072-w.
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spelling pubmed-100125552023-03-15 Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence Khezri, Mohammad Rafi Mohebalizadeh, Mehdi Ghasemnejad-Berenji, Morteza Cell Commun Signal Review Alzheimer’s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated tau proteins. Increasing evidence suggest that targeting the process of Aβ production to reduce its deposition can serve as a therapeutic option for AD management. In this regard, therapeutic interventions shown that a disintegrin and metalloproteinase domain-containing protein (ADAM) 10, involved in non-amyloidogenic pathway of amyloid precursor protein processing, is known to be a suitable candidate. Therefore, this review aims to examine the molecular properties of ADAM10, its role in AD, and introduce it as a therapeutic target to reduce the progression of the disease. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01072-w. BioMed Central 2023-03-14 /pmc/articles/PMC10012555/ /pubmed/36918870 http://dx.doi.org/10.1186/s12964-023-01072-w Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Khezri, Mohammad Rafi
Mohebalizadeh, Mehdi
Ghasemnejad-Berenji, Morteza
Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title_full Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title_fullStr Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title_full_unstemmed Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title_short Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
title_sort therapeutic potential of adam10 modulation in alzheimer’s disease: a review of the current evidence
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10012555/
https://www.ncbi.nlm.nih.gov/pubmed/36918870
http://dx.doi.org/10.1186/s12964-023-01072-w
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