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Psychotic Symptoms in Alzheimer's Disease Are Not Associated With More Severe Neuropathologic Features

Published online by Cambridge University Press:  10 January 2005

Robert A. Sweet
Affiliation:
Division of Geriatrics and Neuropsychiatry, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Ronald L. Hamilton
Affiliation:
Division of Neuropathology, Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Oscar L. Lopez
Affiliation:
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
William E. Klunk
Affiliation:
Division of Geriatrics and Neuropsychiatry, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Stephen R. Wisniewski
Affiliation:
Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA.
Daniel I. Kaufer
Affiliation:
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Matthew T. Healy
Affiliation:
Division of Geriatrics and Neuropsychiatry, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Steven T. DeKosky
Affiliation:
Division of Geriatrics and Neuropsychiatry, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

Abstract

Psychotic symptoms in Alzheimer's disease (AD) have been associated with increased rates of cognitive impairment and functional decline. Prior studies have been conflicting with regard to whether AD patients with psychosis (AD+P) have evidence of more severe neuropathologic findings at postmortem exam. We examined the severity of neuritic plaques and neurofibrillary tangles in six brain regions—middle frontal cortex, hippocampus, inferior parietal cortex, superior temporal cortex, occipital cortex, and transentorhinal cortex—in 24 AD+P subjects and 25 matched AD subjects without psychosis (AD-P). All analyses controlled for the presence of cortical Lewy bodies, and corrected for multiple comparisons. We found no significant associations between neuritic plaque and neurofibrillary tangle severity and AD+P, and no significant associations with any individual psychotic symptom. The association of AD+P with a more rapidly progressive course of AD appears to be mediated by a neuropathologic process other than increased severity of plaque and tangle formation.

Type
Articles
Copyright
© 2000 International Psychogeriatric Association

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