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Interactions between amyloid, amyloid precursor protein, and mitochondria

Mitochondrial dysfunction and Aβ accumulation are hallmarks of Alzheimer's disease (AD). Decades of research describe a relationship between mitochondrial function and Aβ production. Amyloid precursor protein (APP), of which Aβ is generated from, is found within mitochondria. Studies suggest Aβ...

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Autor principal: Wilkins, Heather M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9987971/
https://www.ncbi.nlm.nih.gov/pubmed/36688439
http://dx.doi.org/10.1042/BST20220518
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author Wilkins, Heather M.
author_facet Wilkins, Heather M.
author_sort Wilkins, Heather M.
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description Mitochondrial dysfunction and Aβ accumulation are hallmarks of Alzheimer's disease (AD). Decades of research describe a relationship between mitochondrial function and Aβ production. Amyloid precursor protein (APP), of which Aβ is generated from, is found within mitochondria. Studies suggest Aβ can be generated in mitochondria and imported into mitochondria. APP and Aβ alter mitochondrial function, while mitochondrial function alters Aβ production from APP. The role these interactions contribute to AD pathology and progression are unknown. Here, we discuss prior research, the rigor of those studies, and the critical knowledge gaps of relationships between APP, Aβ, and mitochondria.
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spelling pubmed-99879712023-03-07 Interactions between amyloid, amyloid precursor protein, and mitochondria Wilkins, Heather M. Biochem Soc Trans Review Articles Mitochondrial dysfunction and Aβ accumulation are hallmarks of Alzheimer's disease (AD). Decades of research describe a relationship between mitochondrial function and Aβ production. Amyloid precursor protein (APP), of which Aβ is generated from, is found within mitochondria. Studies suggest Aβ can be generated in mitochondria and imported into mitochondria. APP and Aβ alter mitochondrial function, while mitochondrial function alters Aβ production from APP. The role these interactions contribute to AD pathology and progression are unknown. Here, we discuss prior research, the rigor of those studies, and the critical knowledge gaps of relationships between APP, Aβ, and mitochondria. Portland Press Ltd. 2023-02-27 2023-01-23 /pmc/articles/PMC9987971/ /pubmed/36688439 http://dx.doi.org/10.1042/BST20220518 Text en © 2023 The Author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Articles
Wilkins, Heather M.
Interactions between amyloid, amyloid precursor protein, and mitochondria
title Interactions between amyloid, amyloid precursor protein, and mitochondria
title_full Interactions between amyloid, amyloid precursor protein, and mitochondria
title_fullStr Interactions between amyloid, amyloid precursor protein, and mitochondria
title_full_unstemmed Interactions between amyloid, amyloid precursor protein, and mitochondria
title_short Interactions between amyloid, amyloid precursor protein, and mitochondria
title_sort interactions between amyloid, amyloid precursor protein, and mitochondria
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9987971/
https://www.ncbi.nlm.nih.gov/pubmed/36688439
http://dx.doi.org/10.1042/BST20220518
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