David R Goldsmith1, Ebrahim Haroon2, Andrew H Miller2, Gregory P Strauss3, Peter F Buckley4, Brian J Miller5. 1. Emory University School of Medicine, Department of Psychiatry and Behavioral Sciences, Atlanta, GA, United States. Electronic address: drgolds@emory.edu. 2. Emory University School of Medicine, Department of Psychiatry and Behavioral Sciences, Atlanta, GA, United States. 3. University of Georgia, Department of Psychology, Athens, GA, United States. 4. Virginia Commonwealth University School of Medicine, Richmond, VA, United States. 5. Augusta University, Department of Psychiatry and Health Behavior, Augusta, GA, United States.
Abstract
INTRODUCTION: Increased inflammatory markers have been found in patients with chronic schizophrenia, and have been associated with negative symptoms. The deficit syndrome is a distinct subtype of schizophrenia, characterized by primary and enduring negative symptoms. METHOD: We measured inflammatory markers in patients with and without deficit schizophrenia and controls. RESULTS: Using multivariate analyses, tumor necrosis factor (TNF)-α and interleukin-6 were associated with the deficit syndrome, and TNF-α predicted blunted affect, alogia, and total negative symptoms. CONCLUSIONS: Findings suggest that deficit schizophrenia subtype is associated with increased inflammation and immunotherapies may be a novel target for negative symptoms.
INTRODUCTION: Increased inflammatory markers have been found in patients with chronic schizophrenia, and have been associated with negative symptoms. The deficit syndrome is a distinct subtype of schizophrenia, characterized by primary and enduring negative symptoms. METHOD: We measured inflammatory markers in patients with and without deficit schizophrenia and controls. RESULTS: Using multivariate analyses, tumor necrosis factor (TNF)-α and interleukin-6 were associated with the deficit syndrome, and TNF-α predicted blunted affect, alogia, and total negative symptoms. CONCLUSIONS: Findings suggest that deficit schizophrenia subtype is associated with increased inflammation and immunotherapies may be a novel target for negative symptoms.
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