title: Increased concentrations of presynaptic proteins in the cingulate cortex of subjects with schizophrenia.
abstract: BACKGROUND
  Cytoarchitectural and neurochemical studies demonstrate disorganization in the cerebral cortex in schizophrenia, which perhaps underlies the severe behavioral disturbances of the disease. This neuronal disarray should be accompanied by synaptic abnormalities. As such, presynaptic proteins have proved valuable indexes of synaptic density and their concentrations have correlated markedly with synaptic loss. Our study sought to determine whether abnormalities exist in the concentrations of presynaptic proteins in the postmortem cerebral cortex of subjects with schizophrenia.
  
  
  METHODS
  Presynaptic protein immunoreactivities were assessed in 4 different cerebrocortical regions derived from 16 elderly controls, 19 elderly subjects with schizophrenia, and 24 subjects with Alzheimer's disease. Tissues were assayed with the monoclonal antibodies EP10 and SP4, which recognize synaptophysin, and the monoclonal antibodies SP6 and SP14, which detect syntaxin and synaptosomal-associated protein-25-kd immunoreactivities, respectively.
  
  
  RESULTS
  In subjects with schizophrenia relative to controls, presynaptic proteins were increased in the cingulate cortex, but were unchanged in the temporal, frontal, and parietal cortices. In contrast, when cases with Alzheimer's disease were compared with controls, presynaptic proteins were decreased in the frontal, temporal, and parietal samples.
  
  
  CONCLUSIONS
  These findings reveal changes in the synaptic organization of the cingulate cortex in schizophrenia relative to other areas examined. These changes are distinct from the deficits in presynaptic proteins observed in Alzheimer's disease.
authors.affiliation: Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.
authors.forename: S M
authors.initials: SM
authors.lastname: Gabriel
authors.forename: V
authors.initials: V
authors.lastname: Haroutunian
authors.forename: P
authors.initials: P
authors.lastname: Powchik
authors.forename: W G
authors.initials: WG
authors.lastname: Honer
authors.forename: M
authors.initials: M
authors.lastname: Davidson
authors.forename: P
authors.initials: P
authors.lastname: Davies
authors.forename: K L
authors.initials: KL
authors.lastname: Davis
mesh_terms: D000544:Alzheimer Disease / Q000175:diagnosis / Q000378:metabolism; D000911:Antibodies, Monoclonal; D014150:Antipsychotic Agents / Q000494:pharmacology / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000737:chemistry* / Q000187:drug effects; D003937:Diagnosis, Differential; D006179:Gyrus Cinguli / Q000737:chemistry* / Q000187:drug effects; D006801:Humans; D007118:Immunoassay; D008565:Membrane Proteins / Q000032:analysis; D009419:Nerve Tissue Proteins / Q000032:analysis*; D010751:Phosphopyruvate Hydratase / Q000032:analysis; D050765:Qa-SNARE Proteins; D012559:Schizophrenia / Q000175:diagnosis* / Q000188:drug therapy / Q000378:metabolism; D013572:Synaptic Vesicles / Q000737:chemistry* / Q000187:drug effects; D016708:Synaptophysin / Q000032:analysis; D050825:Synaptosomal-Associated Protein 25
chemical_list: D000911:Antibodies, Monoclonal; D014150:Antipsychotic Agents; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D050765:Qa-SNARE Proteins; C494208:SNAP25 protein, human; D016708:Synaptophysin; D050825:Synaptosomal-Associated Protein 25; D010751:Phosphopyruvate Hydratase