The data available for PD and for AD suggest a pharmacologic profile of rasagiline compatible with either disease modification or symptomatic improvement or both. Enhanced mitochondrial function and improved dopamine neurotransmitter function would be anticipated to provide symptomatic benefit whereas the antiapoptotic neuroprotective activity of rasagiline would be expected to provide disease modification. The proposed clinical trial will not resolve whether one or both of these important therapeutic modalities are predominant. The clinical trial is designed to demonstrate if there is enhanced metabolism in a treatment group compared to a placebo-control. The mechanism of rasagiline is highly supportive of an effect on AD with aspects such as modulation of APP metabolism uniquely relevant to AD.