This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

D. Larry Sparks, PhD; Van M. Woeltz, MD; William R. Markesbery, MD

Arch Neurol. 1991;48(7):718-721.

Abstract
• Alzheimer's disease (AD) and Pick's disease (PD) are dementing disorders of unknown origin. Monoamine oxidase (MAO) is important in the metabolism of a number of monoamine neurotransmitters. This study investigates MAO activity in aging, AD, and PD in frontal and temporal poles, nucleus basalis of Meynert (nbM), and hypothalamus. Regional variations in the activity of the two MAO forms (A and B) were found in aging, AD, and PD. Age-related increase of MAO-B was found in all four areas of the brain, and MAO-A was increased in the nbM and temporal pole. In AD, MAO-B was decreased in the nbM and increased in the temporal pole, while MAO-A was increased in the hypothalamus and frontal pole. In PD, MAO-B was decreased in the nbM and increased in the hypothalamus, while MAO-A was increased in the hypothalamus and decreased in the nbM and temporal pole. These data indicate that with regard to MAO activity, AD and PD are dissimilar diseases and neither strictly follows age-related changes.

Author Affiliations
From the Departments of Pathology, Neurology, and the Alzheimer's Disease Research Center/Sanders-Brown Center on Aging, University of Kentucky Medical Center (Drs Sparks, Woeltz, and Markesbery); and the Kentucky State Medical Examiners Program, Justice Cabinet (Dr Sparks), Lexington.

Footnotes
Accepted for publication November 2, 1990.

Reprint requests to 203 Sanders-Brown Bldg, University of Kentucky Medical Center, Lexington, KY 40536-0230 (Dr Sparks).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

A systematic review of neurotransmitter deficits and treatments in frontotemporal dementia
Huey et al.
Neurology 2006;66:17-22.
ABSTRACT | FULL TEXT  

Molecular Changes Underlying Reduced Pineal Melatonin Levels in Alzheimer Disease: Alterations in Preclinical and Clinical Stages
Wu et al.
J. Clin. Endocrinol. Metab. 2003;88:5898-5906.
ABSTRACT | FULL TEXT  

Presenile dementia syndromes: an update on taxonomy and diagnosis
Greicius et al.
J. Neurol. Neurosurg. Psychiatry 2002;72:691-700.
ABSTRACT | FULL TEXT  

Behavior and treatment in frontotemporal dementia
Perry and Miller
Neurology 2001;56:S46-51.
ABSTRACT | FULL TEXT  

Predominant Expression of Monoamine Oxidase B Isoform in Rabbit Renal Proximal Tubule: Regulation By I2 Imidazoline Ligands in Intact Cells
Gargalidis-Moudanos et al.
Mol. Pharmacol. 1997;51:637-643.
ABSTRACT | FULL TEXT  

High-Dose Selegiline in Treatment-Resistant Older Depressive Patients
Sunderland et al.
Arch Gen Psychiatry 1994;51:607-615.
ABSTRACT  

Altered Serotonergic and Cholinergic Synaptic Markers in Pick's Disease
Sparks and Markesbery
Arch Neurol 1991;48:796-799.
ABSTRACT