Figure 1 Extrinsic and intrinsic pathways of apoptosis. The extrinsic apoptotic pathway is triggered by the binding of a particular death ligand to death receptor, leading to its trimerization and the consequent recruitment of procaspase-8, which is subsequently activated. In contrast, the intrinsic apoptotic pathway starts in response to apoptotic stimuli that induce pro-apoptotic proteins, such as B-cell lymphoma 2-associated X protein (Bax), triggering the permeabilization of the outer mitochondrial membrane, and the consequent release of cytochrome c into the cytosol, where it contributes to the formation of a multimeric apoptotic peptidase activating factor 1 (Apaf-1)/cytochrome c complex that recruits procaspase-9, forming the apoptosome. Hence, procaspase-9 is activated and consequently detached from the complex. Ultimately, active caspase-8 and active caspase-9 activate executioner caspases-3, -6, and/or -7, which mediate apoptosis. This figure was adapted with permission from John Wiley and Sons, from “Apoptosis and its therapeutic implications in neurodegenerative diseases” by Nour S. Erekat, 2022, Clinical Anatomy [34].