Neuronal apoptosis pathways

Neuronal apoptosis pathways refer to the programmed cell death mechanisms that occur within the nervous system, essential for sculpting the brain during development but pathologically activated in disease states (NIH, https://pubmed.ncbi.nlm.nih.gov/11511754/). These pathways are primarily categorized into the intrinsic (mitochondrial) pathway, regulated by the Bcl-2 protein family, and the extrinsic (death receptor) pathway, both of which culminate in the activation of executioner caspases like caspase-3 (StatPearls, https://www.ncbi.nlm.nih.gov/books/NBK537209/). In neurodegenerative conditions such as Alzheimer's and Parkinson's diseases, chronic cellular stress leads to the inappropriate triggering of these pathways, resulting in progressive neuronal loss and functional decline (PubMed, https://pubmed.ncbi.nlm.nih.gov/12467366/). Pharmacological intervention aims to stabilize mitochondrial membranes or inhibit caspase activity to preserve neuronal populations, though achieving cell-type specificity remains a significant challenge (PubMed, https://pubmed.ncbi.nlm.nih.gov/15121113/). Because apoptosis is a fundamental mechanism for eliminating damaged or cancerous cells, systemic inhibition of these pathways carries risks of tumorigenesis and other off-target effects.

Other names

Neuronal programmed cell deathNeuronal apoptotic signalingNeuronal cell death pathways

Modulation of pro-apoptotic signaling molecules such as caspases and BAX, or stabilization of mitochondrial membranes to prevent the release of pro-apoptotic factors like cytochrome c.