Alzheimer's disease is a debilitating neurological disorder which has been predicted to afflict as much as 10 percent of the aged population over 85 years. The disease is characterised by the presence of senile plaques and neurofibrillary tangles, and by widespread neurochemical alterations throughout the brain. The initial event in neurochemical transmission involves the interaction of neurotransmitters with specific receptors. In the majority of cases the modulation of cellular activities by receptor activation is controlled by guanine nucleotide binding proteins (G-proteins). G-proteins are located on the intracellular membrane and respond to receptor stimulation to modulate a variety of signal transduction pathways. Thus, effective therapies targeted at the neurochemical deficits in Alzheimer's disease requires G-protein function to be maintained. This thesis examined the integrity of G-protein mediated signal transduction activities in Alzheimer's disease.