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October 1, 1993

Neurotransmitters in basal ganglia and cortex of Alzheimer's disease with and without Lewy bodies

October 1993 issue
43 (10) 1927

Abstract

We measured the concentrations of the monoamines, their precursors, and their metabolites, and the activity of choline acetyltransferase (ChAT) in basal ganglia and cortical regions of postmortem brains from cases with histologically verified pure Alzheimer's disease (AD), AD with diffusely distributed Lewy bodies (Lewy body variant [LBV]), and normal controls. Dopamine and homovanillic acid (HVA) were severely depleted in basal ganglia of the LBV cases but were not significantly altered in pure AD cases; tyrosine hydroxylase levels in putamen were also significantly reduced in LBV but not AD cases. These reductions in basal ganglia dopamine and HVA suggest that LBV cases have a level of dopamine depletion similar to Parkinson's disease (PD). Additionally, ChAT activity in caudate and norepinephrine concentration in putamen were significantly reduced in the LBV group, which may have contributed to the absence of resting tremor and the milder presentation of parkinsonian features in this group compared with classic PD. In frontal, parietal, and temporal cortex, activity of ChAT in the LBV group was significantly reduced compared with controls and lower than in pure AD.

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Published In

Neurology®
Volume 43Number 10October 1993
Pages: 1927
PubMed: 8105420

Publication History

Published online: October 1, 1993
Published in print: October 1993

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Authors

Affiliations & Disclosures

P. J. Langlais, PhD
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.
L. Thai, MD
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.
L. Hansen, MD
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.
D. Galasko, MD
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.
M. Alford, BA
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.
E. Masliah, MD
From the Department of Neurosciences (Drs. Langlais, Thal, Hansen, Galasko, and Masliah, and M. Alford), University of California at San Diego, School of Medicine; the Neurology Research Service (Drs. Langlais, Thai, and Galasko), Veterans Affairs Medical Center; and the Department of Psychology (Dr. Langlais), San Diego State University, San Diego, CA.

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