Mitochondrial dysfunction is an early, crucial component of cell death in AD. Dysregulated OXPHOS, including the dysfunction of the ATP synthase, induces decreased ATP production and increased ROS. This will ultimately lead to a rise in the rates of apoptotic cell death not only in neurons but also in other cell types in the central nervous center. The increased death of cells will induce serious damage in the brains of the patients, which correlates with the symptoms of the disease. Interestingly, mitochondrial dysfunction, including dysregulated OXPHOS, is an early event in AD, preceding the accumulation of Aβ and the presence of NTFs. ↑ upregulated; ↓ downregulated.