Abstract
Senile dementia of Alzheimer type (SDAT) is a disease of mid- or late life, and about 3 to 4% of the population above 65 years of age is estimated to be afflicted by this progressive dementia.’ One of the main characteristics of this disease is a decline in such cognitive abilities as memory and learning.’ The decline in recent memory seems to be a common characteristic of aging in mammals including humans, non-human primates, and rodents. In humans, this impairment is exacerbated by SDAT. Although the reasons for this cognitive loss in aged or demented subjects are not fully understood, there is evidence that deficits in central cholinergic transmission play an important role.1,3 Postmortem samples from cortical regions of Alzheimer’s Disease (AD) patients have shown decreases of greater than 50% in the activity of choline acetyltransferase (ChAT), the enzyme that catalyzes the final step in the synthesis of acetylcholine (ACh). Scopolamine, an anticholinergic agent, causes memory defects in young adult volunteers. Physostigmine causes memory and thinking disturbances in human volunteers by preventing the hydrolysis of ACh, which accumulates to reach inhibitory concentrations at muscarinic receptors.