Presentation Abstract

Program#/Poster#: 529.2/I27
Title: Nicotine treatment of mild cognitive impairment (MCI): A six-month multi-center pilot study
Location: South Hall A
Presentation Time: Tuesday, Oct 20, 2009, 9:00 AM -10:00 AM
1Clin. Neurosci Res. Unit, Univ. Vermont Col. Med., Burlington, VT; 2Duke Univ., Durham, NC; 3Georgetown Univ., Washington, DC; 4Cognitive Drug Res. Ltd, Goring-on-Thames, United Kingdom
Abstract: Interest in nicotinic treatment of Alzheimer’s disease (AD) developed following recognition of the loss of nicotinic receptors and that short-term administration of nicotine improved cognitive performance in AD. Mild Cognitive Impairment (MCI) may also be an appropriate target for nicotinic treatment as patients will have greater numbers of nicotinic receptors than AD patients. We hypothesized that nicotine treatment would improve cognitive performance and clinical ratings, and that treatment would be safe and well tolerated. 74 non-smoking subjects from 3 sites who met criteria for amnestic MCI were randomized to receive either double-blind transdermal nicotine (15 mg/day) or placebo patch for the first 6 months of the study and open label nicotine patch for the second 6 months of the study. Subjects were cognitively assessed at baseline, 91, and 182 days utilizing the Cognitive Drug Research battery, Conners continuous performance task (CPT), non-computer verbal and visual tasks, and clinical global impression of change (CGIC). For cognitive performance, analysis showed that nicotine treatment produced significant (p<.05) improvements in delayed word recall accuracy, speed of memory, choice reaction time accuracy from the CDR battery, and CPT accuracy and reaction time standard error. In addition, several other cognitive measures including quality of episodic memory and digit symbol substitution task showed strong trends (p<.1) in favor of nicotine treatment. Immediate recall on the paragraph recall task favored placebo. The CGIC results showed that a greater proportion of patients on nicotine were rated as improved compared to the placebo group (23% nicotine vs. 9% placebo and pooling the CGIC results into ‘improvement’, ‘no change’, and ‘worsening’ showed a trend in favor of nicotine (p=0.18). Subject self-ratings of cognitive impairment and alertness showed a strong trend (p<.07) in favor of nicotine. Adverse events were evenly split between nicotine and placebo treatment. Predictably, weight showed a small but significant decline on nicotine (p=0.02) within the first 3 months, as weight between days 91 and 182 was stable. Nicotine significantly (p=.02) reduced systolic blood pressure compared to placebo. Nicotine treatment showed significant improvements in measures of memory and speed with several other measures also showing strong trends towards improvement. The CGIC scores favored nicotine. Treatment in this non-smoking older population was extremely well tolerated. We conclude that transdermal nicotine treatment has significant promise as a symptomatic treatment for amnestic MCI and deserves further exploration in a larger trial.
Disclosures:   P.A. Newhouse, Aventis, C. Other Research Support (receipt of drugs, supplies, equipment or other in-kind support); Pfizer, C. Other Research Support (receipt of drugs, supplies, equipment or other in-kind support); E. Levin, None; H. White, None; E. Coderre, None; H. Wilkins, None; K. Kellar, None; P. Aisen, None; B.K. Saxby, None; K. Wesnes, None.
Keyword(s): NICOTINE
Support: NIA R01 AG022462
[Authors]. [Abstract Title]. Program No. XXX.XX. 2009 Neuroscience Meeting Planner. Chicago, IL: Society for Neuroscience, 2009. Online.

2009 Copyright by the Society for Neuroscience all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.

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