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Interactions between amyloid, amyloid precursor protein, and mitochondria

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BIOCHEMICAL SOCIETY TRANSACTIONS
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PORTLAND PRESS LTD
DOI: 10.1042/BST20220518

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Mitochondrial dysfunction and Aβ accumulation are characteristic features of Alzheimer's disease. Previous research suggests a relationship between the protein APP and Aβ with mitochondrial function, and that changes in mitochondrial function can affect the production of Aβ from APP. The role of these interactions in AD pathology and progression remains unclear. This article discusses the reliability of prior studies and the critical gaps in knowledge regarding the relationships between APP, Aβ, and mitochondria.
Mitochondrial dysfunction and A beta accumulation are hallmarks of Alzheimer's disease (AD). Decades of research describe a relationship between mitochondrial function and A beta production. Amyloid precursor protein (APP), of which A beta is generated from, is found within mitochondria. Studies suggest A beta can be generated in mitochondria and imported into mitochondria. APP and A beta alter mitochondrial function, while mitochondrial function alters A beta 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, A beta, and mitochondria.

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