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Amyloid Precursor Protein (APP) processing to amyloid beta (Aβ) is a major hallmark of Alzheimer's disease (AD). The amyloid cascade hypothesis postulates that accumulation and aggregation causes AD, however many therapeutics targeting have failed recently. Decades of research describe metabolic deficits in AD. Mitochondrial dysfunction is observed in AD subjects within the brain and systemically. APP and γ-secretase are localized to mitochondria. APP can be processed within mitochondria and its localization to mitochondria affects function. Here we discuss the evidence showing APP and γ-secretase localize to mitochondria. We also discuss the implications for the function of APP and its cleavage products in regulating mitochondrial function. Copyright © 2022 Elsevier Ltd. All rights reserved.


Taylor A Strope, Heather M Wilkins. Amyloid precursor protein and mitochondria. Current opinion in neurobiology. 2023 Feb;78:102651

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PMID: 36462447

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