Apoptosis pathways in neurons

The term "apoptosis pathways in neurons" refers to the collection of molecular signaling processes that orchestrate programmed cell death in neuronal cells. These include: - The intrinsic (mitochondrial) pathway, regulated by pro- and anti-apoptotic BCL-2 family proteins and initiated by intracellular stresses (e.g., DNA damage, oxidative stress) leading to mitochondrial outer membrane permeabilization, cytochrome c release, apoptosome formation (APAF1 plus caspase-9), and activation of downstream effector caspases (mainly caspase-3 and caspase-7)[3][4][6]. - The extrinsic (death receptor) pathway, triggered by ligand binding (such as Fas ligand or TNF-α) to death domain-containing receptors (e.g., Fas receptor, TNF receptor, DR4, DR5), leading to assembly of death-inducing signaling complexes and initiation of the caspase cascade via caspase-8 or -10[1][3]. - Both pathways converge on a common set of effector caspases that enact the characteristic morphological and biochemical features of apoptosis, including DNA fragmentation, cell shrinkage, and membrane blebbing[1][2][3][4][6]. Dysregulation of these pathways is central to the pathology of many neurodegenerative diseases (due to excessive apoptosis) and brain cancers (due to evasion of apoptosis), as well as abnormal nervous system development if apoptosis is insufficient or excessive during key developmental windows[3][5][6][7]. Note: For pharmaceutical or mechanistic annotation, refer instead to individual molecular targets within these pathways, such as "Caspase-3", "BCL-2 family protein", or "Fas receptor" for proper structured metadata.

Other names

Apoptotic signaling pathways in neuronsNeuronal apoptosis pathwaysNeuronal programmed cell death pathways