Thompson P M, Sower A C, Perrone-Bizzozero N I
Department of Psychiatry, University of New Mexico School of Medicine, Albuquerque 87131, USA.
Biol Psychiatry. 1998 Feb 15;43(4):239-43. doi: 10.1016/S0006-3223(97)00204-7.
Identifying brain changes in schizophrenia has been a major research focus for many years. Although impressive gains have been made in neuroimaging and brain electrophysiology, molecular and cellular markers of schizophrenia have lagged. There are no consistent biochemical markers for schizophrenia pathophysiology and none that reflect treatment course.
Samples were obtained from 25 postmortem schizophrenic brains and 31 nonschizophrenic controls. These samples were processed, and the synaptosomal fraction was isolated. Ten micrograms of protein from each of these samples was solubilized in a sodium dodecylsulfate sample buffer and separated on 10% (wt/vol) polyacrylamide gels. Monoclonal antibody (SMI-81) was incubated with the blots and, using quantitative Western blotting, we measured the relative amounts of SNAP-25 in these samples.
We report altered levels of SNAP-25 in both the inferior temporal cortex (Brodmann area 20) and prefrontal association cortex (Brodmann areas 9 and 10) in postmortem brains of patients with schizophrenia relative to nonschizophrenic controls. Normal levels of SNAP-25 are noted in schizophrenics in area 17, decreased levels in areas 10 and 20, and an elevated level in area 9.
These data support cytoarchitectural observations that the cerebral cortex of schizophrenic patients has extensive pathology. The data presented here, along with data on other brain-specific proteins, indicate a complicated molecular adaptation to the causative factors of schizophrenia.
