It is a relatively new investigative tool that will likely be used more in the next few years, particularly in conjunction with functional measures of the brain. Implications and future directions for research Based on a review of structural neuroimaging studies in schizophrenia, it is clear that schizophrenia is a brain disorder that shows marked, albeit subtle, neuroanatomical abnormalities that are multifocal in nature and which likely involve brain circuits and Inhibitors,research,lifescience,medical networks which subserve cognition and behavior. Evidence also suggests that schizophrenia involves a disorder of neural and cognitive integration, an idea that has long been proposed in the schizophrenia literature. Some

of the more recent theories that touch upon disordered integration include the dysmetria theory proposed by Andreasen et al,70 the failure of integration proposed by Gruzelier et al,71 Feinberg’s30 theory of aberrant synaptic pruning, Friston’s72

theory of abnormal synaptic modulation, and Bartzokis’s73 theory Inhibitors,research,lifescience,medical which suggests that the underlying cause of neural integration may be abnormalities in myelination processes that occur in the periadolescent period. Inhibitors,research,lifescience,medical Despite promising findings, however, we are still far from understanding the neuropathology of schizophrenia. Some of the outstanding questions that remain to be addressed if we are to understand the etiology of schizophrenia are: When do structural brain abnormalities first occur? What are the microstructural underpinnings Inhibitors,research,lifescience,medical of these structural brain abnormalities? Is there a causative relationship between gray matter abnormalities free overnight delivery observed with MRI and white matter abnormalities observed with DTI? Do all of the structural brain abnormalities associated with schizophrenia progress with illness, or are some stable over time? Is it possible to arrest these Romidepsin mw progressive neuroanatomical changes once they have begun? As brain abnormalities in patients with schizophrenia have been shown to be associated with cognitive and clinical

symptoms, how do Inhibitors,research,lifescience,medical we understand improvement in cognitive and clinical symptoms which are often concomitant with progressive volume reductions following the first episode of illness? What is the relationship between the structural brain abnormalities characteristic of schizophrenia and the equally well documented functional Anacetrapib brain abnormalities (eg, such as observed with PET, fMRI, etc)? Can neuroanatomical, neuropsychological, or clinical phenotypes be used to predict who will go on to develop schizophrenia and who will not? These are among the questions that we need to address in future studies. While these questions are daunting, there is nonetheless reason for optimism. The technological advances in neuroimaging that have led to new discoveries about the brain and its role in schizophrenia will continue.