ABSTRACT
Neuroscience Research Institute, University of Ottawa, 451 Smyth Rd. Ottawa, ON K1H 8M5, Canada
Apoptotic cell death, with its characteristic morphological features, plays an important role in a diverse range of biological processes (reviewed in Wyllie et al., 1980). One major focus of this field has been to define and order the elements that control this type of death. It has become clear that cell death pathways consist of a conserved class of molecules typified by the Ced 3, 4, and 9 genes (reviewed in Jacobson et al., 1997) as well as a myriad of other signaling events which may depend upon cell context and the particular apoptotic initiator. These elements are ordered in a series of multistep signaling events which control apoptotic death (Park et al., 1997b; see Figure 10.1). Hence, one biochemical view of apoptotic regulation is that a variety of stimuli initiate apoptosis death by activating a wide range of upstream effector signaling events. These events are somehow integrated to control the time of cell death via activation of the caspases. Once the caspases are activated, they initiate a series of downstream events that irreversibly lead to cell death. In this brief summary, we will discuss some findings that relate to this general model and discuss the implications of these results in identifying potential molecular targets for therapeutic intervention in brain injury and neurodegenerative diseases.
