The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology

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• dc.contributor.author Fanlo-Ucar, Hugo
• dc.contributor.author Picón-Pagès, Pol
• dc.contributor.author Herrera Fernández, Víctor
• dc.contributor.author Ill-Raga, Gerard, 1982-
• dc.contributor.author Muñoz López, Francisco José, 1964-
• dc.date.accessioned 2025-03-26T07:32:49Z
• dc.date.available 2025-03-26T07:32:49Z
• dc.date.issued 2024
• dc.description.abstract Alzheimer's disease (AD) is a progressive neurodegenerative disease, and it is currently the seventh leading cause of death worldwide. It is characterized by the extracellular aggregation of the amyloid β-peptide (Aβ) into oligomers and fibrils that cause synaptotoxicity and neuronal death. Aβ exhibits a dual role in promoting oxidative stress and inflammation. This review aims to unravel the intricate connection between these processes and their contribution to AD progression. The review delves into oxidative stress in AD, focusing on the involvement of metals, mitochondrial dysfunction, and biomolecule oxidation. The distinct yet overlapping concept of nitro-oxidative stress is also discussed, detailing the roles of nitric oxide, mitochondrial perturbations, and their cumulative impact on Aβ production and neurotoxicity. Inflammation is examined through astroglia and microglia function, elucidating their response to Aβ and their contribution to oxidative stress within the AD brain. The blood-brain barrier and oligodendrocytes are also considered in the context of AD pathophysiology. We also review current diagnostic methodologies and emerging therapeutic strategies aimed at mitigating oxidative stress and inflammation, thereby offering potential treatments for halting or slowing AD progression. This comprehensive synthesis underscores the pivotal role of Aβ in bridging oxidative stress and inflammation, advancing our understanding of AD and informing future research and treatment paradigms.
• dc.description.sponsorship This work was supported by the Spanish Ministry of Science, Innovation and Universities (MCIU) and the Agencia Estatal de Investigación (AEI) plus European Social Fund Plus (FSE+) through grant PID2020-117691RB-I00/AEI/10.13039/501100011033 and PID2023-149767OB-I00 with the reference MCIU/AEI/10.13039/501100011033 plus FSE+. This work was also funded by the “María de Maeztu Programme” for Units of Excellence in Research and Development (R&D; award CEX2018-000792-M).
• dc.format.mimetype application/pdf
• dc.identifier.citation Fanlo-Ucar H, Picón-Pagès P, Herrera-Fernández V, Ill-Raga G, Muñoz FJ. The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology. Antioxidants (Basel). 2024 Oct 8;13(10):1208. DOI: 10.3390/antiox13101208
• dc.identifier.doi http://dx.doi.org/10.3390/antiox13101208
• dc.identifier.issn 2076-3921
• dc.identifier.uri http://hdl.handle.net/10230/70015
• dc.language.iso eng
• dc.publisher MDPI
• dc.relation.ispartof Antioxidants (Basel). 2024 Oct 8;13(10):1208
• dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/PID2020-117691RB-I00
• dc.relation.projectID info:eu-repo/grantAgreement/ES/3PE/PID2023-149767OB-I00
• dc.relation.projectID info:eu-repo/grantAgreement/ES/2PE/CEX2018-000792-M
• dc.rights © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword Alzheimer’s disease
• dc.subject.keyword BACE1
• dc.subject.keyword Amyloid β-peptide
• dc.subject.keyword Neurodegeneration
• dc.subject.keyword Nitro-oxidative stress
• dc.title The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion