Extended-Release Physostigmine in Alzheimer Disease

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Abstract
ALZHEIMER DISEASE (AD) is a progressive neurodegenerative disease that affects an estimated 4.5 million Americans.1 It exacts a formidable emotional and financial toll on patients, caregivers, and society—with annual treatment costs in the United States as high as $100 billion.2 Although the etiology of AD remains unknown, several lines of evidence have implicated a decline in central cholinergic neurotransmission as a critical event in cognitive dysfunction in AD. Postmortem brains with AD demonstrate an extensive loss of cholinergic neurons in the nucleus basalis of Meynert that project widely to neocortex, amygdala, and hippocampus.3,4 Reduced activity of cortical choline acetyltransferase, the enzyme that synthesizes acetylcholine, correlates with the number of senile plaques and with cognitive impairment in patients with AD.5