The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology
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....
| Autores: | , , , , |
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| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | España |
| Recursos: | Universitat Pompeu Fabra |
| Repositorio: | Repositorio Digital de la UPF |
| OAI Identifier: | oai:repositori.upf.edu:10230/70015 |
| Acesso em linha: | http://hdl.handle.net/10230/70015 http://dx.doi.org/10.3390/antiox13101208 |
| Access Level: | acceso abierto |
| Palavra-chave: | Alzheimer’s disease BACE1 Amyloid β-peptide Neurodegeneration Nitro-oxidative stress |
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The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology Fanlo-Ucar, Hugo Picón-Pagès, Pol Herrera Fernández, Víctor Ill-Raga, Gerard, 1982- Muñoz López, Francisco José, 1964- Alzheimer’s disease BACE1 Amyloid β-peptide Neurodegeneration Nitro-oxidative stress 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. 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). MDPI http://hdl.handle.net/10230/70015 http://dx.doi.org/10.3390/antiox13101208 |
| title |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| spellingShingle |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology Fanlo-Ucar, Hugo Alzheimer’s disease BACE1 Amyloid β-peptide Neurodegeneration Nitro-oxidative stress |
| title_short |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| title_full |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| title_fullStr |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| title_full_unstemmed |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| title_sort |
The dual role of amyloid beta-peptide in oxidative stress and inflammation: Unveiling their connections in Alzheimer's disease etiopathology |
| author |
Fanlo-Ucar, Hugo |
| author_facet |
Fanlo-Ucar, Hugo Picón-Pagès, Pol Herrera Fernández, Víctor Ill-Raga, Gerard, 1982- Muñoz López, Francisco José, 1964- |
| author_role |
author |
| author2 |
Picón-Pagès, Pol Herrera Fernández, Víctor Ill-Raga, Gerard, 1982- Muñoz López, Francisco José, 1964- |
| author2_role |
author author author author |
| topic |
Alzheimer’s disease BACE1 Amyloid β-peptide Neurodegeneration Nitro-oxidative stress |
| topic_facet |
Alzheimer’s disease BACE1 Amyloid β-peptide Neurodegeneration Nitro-oxidative stress |
| description |
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. |
| publishDate |
2024 |
| format |
article |
| status_str |
publishedVersion |
| url |
http://hdl.handle.net/10230/70015 http://dx.doi.org/10.3390/antiox13101208 |
| eu_rights_str_mv |
openAccess |
| publisher |
MDPI |
| institution |
Universitat Pompeu Fabra |
| collection |
Repositorio Digital de la UPF |
| reponame_str |
Repositorio Digital de la UPF |
| instname_str |
Universitat Pompeu Fabra |
| _version_ |
1878736459797626880 |
| publishDateSort |
2024 |
| author_browse |
Fanlo-Ucar, Hugo Herrera Fernández, Víctor Ill-Raga, Gerard, 1982- Muñoz López, Francisco José, 1964- Picón-Pagès, Pol |
| publisherStr |
MDPI |
| score |
6,9008884 |