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In this issue

In their review, Duffy et al. examine the evidence implicating mitochondria in the aetiology and pathogenesis of amyotrophic lateral sclerosis (ALS). Mitochondria are the sites of oxidative phosphorylation within the cell and also have a central role in apoptosis cascades. They are dynamic structures, undergoing fission and fusion, and forming branching networks. Their transport within the neuron is essential to generation of energy throughout the cell. This review examines the alterations in the morphology, function and axonal transport of mitochondria associated with human ALS and in experimental models, and examines the potential therapeutic targets associated with the abnormalities of this organelle.