Neurodegenerative disorders such as Alzheimer's, Parkinson's and Huntington's diseases affect millions of people. These disorders are age-dependent, progressive and, at present, incurable. A practical and relevant model is needed to investigate the molecular determinants of these debilitating diseases. Mammalian models are often prohibitively expensive, time-consuming and very complex. Given the highly conserved neurological pathways between mammals and invertebrates, Caenorhabditis elegans has emerged as a powerful tool for the investigation of the pathophysiology of these disorders. We describe recent findings in this area and show how C. elegans is being used to broaden our knowledge of human neurodegenerative diseases.

Acute exposure to ethanol is known to modulate signalling within the nervous system. Physiologically these effects are both presynaptic and postsynaptic in origin; however, considerably more research has focused primarily on postsynaptic targets. Recent research using the model organism Caenorhabditis elegans has determined a role for specific proteins (Munc18-1 and Rab3) and processes (synaptic vesicle recruitment and fusion) in transducing the presynaptic effects of ethanol. In the present paper, we review these results, identifying the proteins and protein interactions involved in ethanol sensitivity and discuss their links with mammalian studies of alcohol abuse.