8-11 These are summarized in Table

I, together with some of the other findings that are of current interest, but that have not been substantiated to the same extent.12,13 Because the focus of this paper is on postmortem studies, the imaging literature is not discussed in detail. However, it is noteworthy that it is the incontrovertible in vivo imaging evidence that there is a pathology of schizophrenia to be found which has driven the ongoing neuropathological studies. Table I. Macroscopic brain changes in schizophrenia. The imaging data have also allowed other important conclusions to be drawn, which inform and bolster postmortem research (Table II). 14-18 In particular, since the structural Inhibitors,research,lifescience,medical changes are present at the time of disease onset and are, by and large, not progressive thereafter (although there may well be exceptions to this rule17,19), it is reasonable to assume that the Inhibitors,research,lifescience,medical corresponding histological abnormalities share this property, even though it is in practice impossible to prove this in postmortem studies. Inhibitors,research,lifescience,medical Instead, the latter can now focus on the microscopic and molecular aspects of the pathology, which remain out of reach of any imaging modality. Table II. Characteristics of structural imaging findings in schizophrenia. Histological and molecular pathology of schizophrenia Contemporary histological studies have addressed two main

areas: first, to clarify the frequency and nature of neurodegenerative abnormalities in schizophrenia; and, second, to investigate the cellular organization (cytoarchitccture) of the brain. A summary of the most established and the most often cited findings Inhibitors,research,lifescience,medical is given in Table III. Table III. Histological findings in schizophrenia. Gliosis

and neurodegeneration The two most robust and important findings concerning the neuropathology of schizophrenia are Inhibitors,research,lifescience,medical both negative: there is no excess of gliosis, or of Alzheimer’s disease or other neurodegenerative pathology. The issue of gliosis (reactive astrocytosis) has been extensively investigated since a report, that gliosis was common in schizophrenia, especially in the diencephalon around the third ventricle.20 As gliosis is a sign of past inflammation, this invoked scenarios for schizophrenia involving infective, Proteasome inhibitor ischemic, autoimmune, or neurodegenerative processes. However, over a dozen subsequent investigations CYTH4 using more quantitative methods have not replicated this observation, and the consensus is now that gliosis is not a feature of schizophrenia.21 The issue is complicated by the excess of nonspecific and focal abnormalities, including gliosis, seen in brain scries of schizophrenia; however, this is likely to be an epiphenomenon not an intrinsic finding21,22 and, importantly, decreased brain size is still seen after omission of all such brains.