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Alzheimer's disease (AD), the most common form of dementia, is a neurodegenerative disorder characterized by a gradual progression of cognitive, functional, and behavioral deficits.1 The disease is currently estimated to affect 4 million people in the United States; however, the prevalence increases with age.2 In those aged 65 years, the prevalence is about 5%; beyond 65, the rate doubles approximately every 5 years.3,4 The typical duration of the disease from onset to death is about 8 to 10 years,5,6 hence affected patients generally require long-term symptomatic treatment. Consequently, long-term data on the safety and efficacy of therapeutic agents are essential in this patient population. Although the exact pathophysiology of AD has not been fully established, the cognitive deficits associated with the disease are primarily related to cholinergic deficits.7 Development of potential therapies has therefore focused on enhancing cholinergic neurotransmission. Cholinesterase inhibitors (ChEIs), which enhance cholinergic function, are the standard pharmacologic treatment for mild-to-moderate AD. The currently available ChEIs, donepezil, rivastigmine, and galantamine, enhance cholinergic function by inhibiting cholinesterases that degrade acetylcholine, thereby increasing the availability of the neurotransmitter to stimulate nicotinic and muscarinic receptors in the brain. They have been shown to improve the cognitive, functional, and behavioral symptoms of AD and are approved for the symptomatic treatment of mild-to-moderate disease8,9; however, donepezil has recently received U.S. Food and Drug Administration approval for the treatment of severe AD. The ChEIs differ in their affinity for acetylcholinesterase and butyrylcholinesterase; donepezil and galantamine are essentially selective for acetylcholinesterase, while rivastigmine inhibits both with similar affinity.10 Rivastigmine differs from the rapidly reversible cholinesterase inhibitors, donepezil and galantamine, in that it is a slowly reversible (pseudo-reversible) ChEI of the carbamate class with brain-regional specificity for the cerebral cortex and hippocampus.10 Although donepezil, rivastigmine, and galantamine belong to different chemical classes, they have shown similar levels of improvement in cognitive function in studies to date8; however, their differing pharmacologic, pharmacokinetic, tolerability, and drug interaction profiles may influence individual treatment response.8,10 It may, therefore, be beneficial to switch between ChEIs if patients fail to respond to treatment, deteriorate, or are unable to tolerate their current treatment.11,12 A recent 26-week open-label study13 showed that switching patients immediately (i.e., without a washout period) to rivastigmine 3 to 12 mg/day after poor response to donepezil improved or stabilized global functioning in almost 70% of patients. The immediate switch was also safe and well tolerated. Patients who completed the 26-week treatment period had the option to continue open-label treatment with rivastigmine for an additional 26 weeks. This report presents the final 52-week safety and tolerability data from this study, as well as outcomes data.