© 1998 by Oxford University Press and the Maryland Psychiatric Research Center (MPRC)
Postmortem Studies in Schizophrenia
Assistant Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Associate Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Assistant Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Assistant Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Professor of Psychiatry and Pathology, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Associate Professor of Psychiatry, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Professor and Chairman, Department of Psychiatry, Mt. Sinai Medical Center New York, NY
Reprint requests should be sent to Dr. P. Powchik, Pfizer, Inc., 235-10-50, 235 East 42nd St., New York, NY 10017
The past decade has seen renewed interest in the neuropathology of schizophrenia. The advent of new postmortem techniques and functional imaging, along with a greater understanding of the neuropsychology of schizophrenia, have provided many new clues to the nature of the underlying brain dysfunction in this disorder. There has also been a greater understanding of the presence of severe cognitive dysfunction among many elderly persons with schizophrenia. In this article, a series of investigations are described that seek to answer basic questions about the neuropathology of schizophrenia, in particular as it pertains to cognitive impairment. The first study describes neuropathological findings in 100 consecutively autopsied persons with schizophrenia, the majority of whom had had detailed antemortem assessments. Results from this first study prompted the conclusion that schizophrenia is not characterized by classical, histologically identifiable neuropathology. Moreover, most cases of dementia in schizophrenia are probably not the result of neuropathologically identifiable dementing illnesses. The next four studies examined chemical markers that are altered in Alzheimer's disease and some other dementing conditions and have also been suggested to be abnormal in schizophrenia: choline acetyltransferase, catecholamines and indolamines, neuropeptides, and synaptic proteins. Schizophrenia cases as a group did not show a cholinergic deficit; nor did they differ from elderly comparison cases with respect to cortical catecholamines and indolamines. Among the schizophrenia cases, however, cognitive impairment was negatively correlated with choline acetyltransferase activity. Those with cognitive impairment showed evidence of cortical noradrenergic and serotonergic deficits. Neuropeptide deficits were also present in schizophrenia, but their pattern differed from that seen in Alzheimer's disease. Increased synaptic protein activity was found in the cingulate cortex of persons with schizophrenia, and this activity was correlated with schizophrenia symptoms. From this second series of studies, it was concluded that some biological measures in schizophrenia may be related to cognitive impairment (e.g., cortical amines), whereas others may be related to diagnosis (e.g., neuropeptide deficits). In addition, synaptic organization may correlate with schizophrenia symptoms.
Keywords: Brain pathology / dementia / serotonin / norepinephrine / synaptic proteins
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