In AD patients and animal models of AD (e.g., APP/PS1 mice), neurons exhibit hallmark mitochondrial defects, including fragmented morphology, elevated mtDNA deletions, and impaired cytochrome c oxidase (COX) activity—a key indicator of oxidative phosphorylation failure (Swerdlow, 2018; Tran and Reddy, 2020). This evidence concerns the gene APP and Alzheimer disease.