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Erich Mohr, PhD; Jerry Schlegel, MD; Giovanni Fabbrini, MD; Jill Williams, MA; M. Maral Mouradian, MD; Ulrike M. Mann, MD; Jules J. Claus, MD; Paul Fedio, PhD; Thomas N. Chase, MD

Arch Neurol. 1989;46(4):376-378.

Abstract
• A loss of cortical noradrenergic innervation may contribute to the intellectual deterioration in Alzheimer's disease. To test the hypothesis that noradrenergic replacement may confer symptomatic benefit, a double-blind, placebo-controlled therapeutic trial with clonidine hydrochloride (Catapres), a centrally active noradrenergic receptor agonist, was undertaken in eight patients with the clinical diagnosis of Alzheimer's disease. No statistically significant changes in cognitive function were found over a range of doses, including those that produced clinically observable side effects. These preliminary results indicate a need for alternative noradrenergic replacement strategies in Alzheimer's disease.

Author Affiliations
From the Medical Neurology Branch (Drs Mohr and Fedio) and the Experimental Therapeutics Branch (Drs Schlegel, Fabbrini, Mouradian, Mann, Claus, and Chase and Ms Williams), National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Md.

Footnotes
Accepted for publication October 1, 1988.

Reprint requests to National Institutes of Health, Bldg 10, Room 5C-416, 9000 Rockville Pike, Bethesda, MD 20892 (Dr Mohr).

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