BCL-2 homologues are major regulators of apoptosis and, as such, play an active role in the survival of adult neurons following injury. In recent years, these proteins have also been associated with the regulation of autophagy, a catabolic process involved in the recycling of nutrients upon starvation. Basal levels of autophagy are also required to eliminate damaged proteins and organelles. This is illustrated by the accumulation of ubiquitin-positive aggregates in cells deficient in autophagy and, in the nervous system, this is associated with progressive cell loss and signs of neurodegeneration. Given the importance of both apoptosis and autophagy for neuronal survival in adult neurons, understanding how BCL-2 homologues co-ordinately regulate these processes will allow a better understanding of the cellular processes leading to neurodegeneration. In the present review, we will discuss the roles of BCL-2 homologues in the regulation of apoptosis and autophagy, focussing on their impact on adult neurons.

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