HOME HELP FEEDBACK SUBSCRIPTIONS ALL ISSUES SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nishioka, N. Articles by Arnold, S. E. Search for Related Content PubMed PubMed Citation Articles by Nishioka, N. Articles by Arnold, S. E.

Evidence for Oxidative DNA Damage in the Hippocampus of Elderly Patients With Chronic Schizophrenia

Received January 2, 2004; revised January 6 2004; accepted January 12, 2004. From the Cellular and Molecular Neuropathology Program, Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA. Send correspondence to Steven E. Arnold, M.D., 547 Clinical Research Bldg., 415 Curie Blvd., Philadelphia, PA 19104. e-mail: sarnold{at}mail.med.upenn.edu
© 2004 American Association for Geriatric Psychiatry

Objective: The authors investigated the idea that some patients with schizophrenia exhibit a chronic, deteriorating course without showing frank neurodegeneration at postmortem examination. Oxidative damage is one form of cellular injury that may cause cellular dysfunction without necessarily leading to neuron death. Methods: Authors obtained postmortem hippocampi from 13 elderly non-psychiatric comparison cases and 10 patients with "poor-outcome" schizophrenia. The groups were compared for the presence of neuronal 8-hydroxy, 2' deoxyguanosine (8-OHdG), a robust marker of oxidized DNA, and neuronal Ki-67, a marker of cell-cycle activation, as well as neurofibrillary tangles, amyloid-beta senile plaques, and astrocytosis. Results: The mean proportion of neurons exhibiting 8-OHdG immunoreactivity was 10 times higher in schizophrenia than in comparison cases. Ki-67 was similarly elevated and was correlated with 8-OHdG in the schizophrenia group. There were no significant between-group differences for densities of neurofibrillary tangles, amyloid-beta plaques, or astrocytes. Conclusions: Our data provide evidence for oxidative DNA damage and coordinated cell-cycle activation in elderly "poor-outcome" schizophrenia. These findings could have important implications for cellular metabolism, gene expression, and membrane functioning in schizophrenia.

Key Words: Neurophysiology • Genetics • Medical Comorbidity • Schizophrenia

This article has been cited by other articles:

				S. E. Arnold Bedside to Bench and Back Again: Translational Neuroscience Research and Geriatric Psychiatry Am J Geriatr Psychiatry, April 1, 2004; 12(2): 122 - 125. [Full Text] [PDF]