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Murray A. Raskind, MD; Carl H. Sadowsky, MD; William R. Sigmund, MD; Paula J. Beitler, PhD; Sheila B. Auster, PhD

Arch Neurol. 1997;54(7):836-840.

Abstract
Objective
To examine the effects of tacrine hydrochloride in patients with Alzheimer disease (AD) and detectable baseline deficits in discrete cognitive and noncognitive parameters who were enrolled in a previously reported multicenter, double-blind, 30-week trial.

Design
An exploratory analysis using last observation carried forward. The study population included a placebo group (n= 181) and all patients randomized to treatment with 160 mg/d of tacrine hydrochloride (n=238), regardless of highest dose achieved or duration of tacrine therapy.

Study Population
Male and female subjects, at least 50 years of age, with mild to moderate AD and detectable baseline deficits in discrete cognitive and noncognitive parameters.

Main Outcome Measures
Change from baseline to last observation carried forward in discrete subscale scores of the Alzheimer's Disease Assessment Scale (ADAS): cognitive (memory, language, praxis) and noncognitive (mood, behavior). Improvement was defined as a decrease of at least 1 point from baseline; stabilization was defined as no change or a decrease from baseline.

Results
Compared with the placebo group, the percentage of patients receiving tacrine whose conditions improved or stabilized was significantly greater for 8 of 11 ADAS-cognitive items (word recall, word recognition, orientation, language production, comprehension, word finding, following commands, ideational praxis) and for the ADAS-noncognitive items: cooperation, delusions, and pacing.

Conclusions
Tacrine stabilizes or improves specific behavioral deficits and symptoms in AD. The previous demonstration of tacrine's effect on global cognitive function has been extended by suggesting an association between tacrine therapy and improvements in individual cognitive and noncognitive items of the ADAS. Effects of tacrine in clinical practice might be more accurately and efficiently assessed by measuring individual ADAS cognitive and noncognitive items relevant to individual patient pretreatment clinical status.

Author Affiliations
From the Veterans Affairs Puget Sound Health Care System and University of Washington School of Medicine, Seattle (Dr Raskind); the Palm Beach Neurological Group, Palm Beach, Fia (Dr Sadowsky); and the Parke-Davis Pharmaceutical Division of Warner-Lambert Co, Morris Plains, NJ (Drs Sigmund, Beitler, and Auster). Dr Raskind is a consultant to Parke-Davis. Drs Sigmund, Beitler, and Auster are employed by and own stock in Parke-Davis Pharmaceutical Division of Warner-Lambert Co.

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