Apoptosis is a form of cellular suicide that allows for the removal of damaged, infected, superfluous or otherwise questionable cells without releasing toxic cellular contents that may trigger an inflammatory response, or damage nearby cells. The active and orderly characteristics of apoptosis contrast with necrotic cell death, which is stochastic and usually pro-inflammatory. The biochemical pathways involved in apoptosis involve the activation of a family of constitutively expressed proteinases called caspases. Working backwards from the last stages of cell death toward caspase activation we can now determine which apoptotic pathways are engaged in response to particular pro-apoptotic stimuli. Among the beneficiaries of this newfound knowledge are those investigators working on neurodegenerative disorders that result from the apoptotic death of discrete neuronal populations. Applying current knowledge of the mechanisms of apoptosis to long-studied disorders such as Huntington's, Parkinson's and Alzheimer's diseases is a bit like turning to the back of a mystery novel halfway through. If the middle chapters of that book are missing, knowing how it ends will aid greatly in reconstructing what happened, despite taking out some of the mystery. The detailed characterization of apoptosis is providing an end-point from which we can trace these disorders backwards to their causes. Insights provided by apoptosis research will speed progress and aid in the development of efficacious treatments that address the causes, rather than just the symptoms, of many neurodegenerative disorders.
