Razadyne® (galantamine hydrobromide), previously Reminyl is the latest cholinesterase inhibitor to be approved in the US. It is taken twice a day like Exelon (rivastigmine), but Aricept is taken once a day. It has been found to improve cognitive test scores and global functioning of people with mild to moderate AD. These improvements were maintained for 12 months. Reminyl boosts the level of acetylcholine in the brain and, unlike other CEI therapies, it affects neural nicotinic receptors*.

"Galantamine significantly reduced behavioural disturbances after 3 months in this population and this had a positive impact on behaviour-related caregiver burden. Galantamine showed the expected safety profile and was well tolerated."
Monsch AU et al Effects of galantamine on behavioural and psychological disturbances and caregiver burden in patients with Alzheimer's disease. Curr Med Res Opin. Jun;20(6):931-8, 2004

Earlier supporting article for references:

Raskind, M. & Truyen, L. Galantamine has Cognitive Benefits for Patients with Alzheimer's Disease after 36 Months of Continuous Treatment. 8th International Conference on Alzheimer's Disease and Related Disorders, Stockholm, Sweden, 20-25 July 2002.
25% of patients showed clinically important improvements at Month 12, and, by month 36, nearly 7% of patients still showed those improvements. Over half improved or maintained cognitive function at Month 12.

Extensive earlier results at:
Raskind, MA, Peskind, ER, Wessel, T et al Neurology, 54, 2261-2268, 2000 and
Doody, RS & Kershaw, P Neurology, 56 (Suppl 3): A456, 2001.

Rockwood K, Mintzer J, Truyen L, Wessel T, Wilkinson D. Effects of a flexible galantamine dose in Alzheimer's disease: a randomised, controlled trial. J Neurol Neurosurg Psychiatry,71(5): 589-95, 2001.
OBJECTIVE: To assess the efficacy and safety of galantamine in Alzheimer's disease at 3 months using flexible dose escalation.
METHODS: A randomised, double blind, placebo controlled trial in 43 centres in the United States, Canada, Great Britain, South Africa, Australia, and New Zealand. Patients with probable Alzheimer's disease (n=386; 171 women) with a score of 11-24 on the mini mental state examination, and a score>/=12 on the cognitive subscale of the Alzheimer's disease assessment scale (ADAS-cog) were randomised to placebo, or galantamine escalated over 4 weeks to a maintenance dose of 24 or 32 mg/day. The primary outcome measures were the change in ADAS-cog score and the clinician's interview based impression of change plus caregiver input (CIBIC-plus) score. Activities of daily living (ADL) and behavioural symptoms were secondary outcomes. To compare the effects of highest levels of dosing, an observed cases (OC) analysis was undertaken, with classic intention to treat (ITT) and ITT with last observation carried forward (LOCF) as confirmatory analyses.
RESULTS: At 3 months, galantamine (24-32 mg/day) produced a significantly better outcome on cognitive function than placebo (treatment difference=1.9 points on ADAS-cog, p=0.002) and a significantly better global response than placebo, as measured by CIBIC-plus (deterioration in 21% of patients on galantamine v 37% on placebo; p<0.001). Galantamine produced significant benefits on basic and instrumental ADL. Behavioural symptoms did not change significantly from baseline levels in either group. Adverse events (primarily gastrointestinal) were of mild to moderate intensity. There were no important differences between the OC, ITT, and ITT/LOCF analyses. Most patients (82%) who were maintained on the higher dose of galantamine completed the study.
CONCLUSIONS: Patients on galantamine, compared with those on placebo, experienced benefits in cognitive function and in the basic activities of daily living. Flexible dose escalation of galantamine was well tolerated.

* Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia. Nicotine and nicotinic agonists have been shown to improve cognitive function in aged or impaired subjects. Smoking has also been shown in some epidemiological studies to be protective against the development of neurodegenerative diseases. This is supported by animal studies that have shown nicotine to be neuroprotective both in vivo and in vitro. Treatment with nicotinic agonists may therefore be useful in both slowing the progression of neurodegenerative illnesses, and improving function in patients with the disease. While increased nicotinic function has been shown to be beneficial, loss of cholinergic markers is often seen in patients with dementia, suggesting that decreased cholinergic function could contribute to both the cognitive deficits, and perhaps the neuronal degeneration, associated with dementia.
Picciotto MR, Zoli M.(Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, Connecticut 06508, USA. marina.picciotto@yale.edu) J Neurobiol 2002 Dec;53(4):641-55.