First, impairments in neurocognition are core features of schizophrenia. These impairments

are present during acute MAPK Inhibitor Library cost exacerbations of the illnesses and during periods of remission. In addition, first- and secondgeneration antipsychotics are relatively ineffective at treating these symptoms. Patients treated with these agents tend to have continuing deficits even when adequately treated with antipsychotics.5 Further, the neurocognitive deficits tend to be relatively severe. A metaanalysis by Heinrichs and Zakzanis6 demonstrates that the impairments in Inhibitors,research,lifescience,medical schizophrenia are particularly severe for memory, attention, and executive function. In these areas, individuals Inhibitors,research,lifescience,medical with schizophrenia – on average – performed 1.5 standard deviations below community norms. The most important, reason for the focus on neurocognition may be that these impairments appear to be related to the functional outcomes of patients. A Inhibitors,research,lifescience,medical review by Green7 found that the impairments in social and vocational functioning in schizophrenia were strongly related to the impairments in neurocognition. The magnitudes for the relationships between cognitive deficits and functional outcome are

medium Inhibitors,research,lifescience,medical for individual cognitive constructs

such as attention or working memory, but the relationships can be strong when summary scores (eg, composites of several cognitive functions) are used.8-10 This literature on cognitive linkages to functional outcome provides a compelling rationale for intervention development at the level of cognition. In contrast, to cognitive deficits, clinical symptoms are only weakly Inhibitors,research,lifescience,medical related to functional outcome in schizophrenia. Facilitating drug development Hyman and Fen ton2 have suggested a strategy for drug development that focuses on dissecting psychiatric disorders into component, dimensions of psychopathology that may be more closely related to pathophysiological processes. These components rather than the illnesses themselves may be more (-)-p-Bromotetramisole Oxalate amenable to novel pharmacological approaches to therapeutics. This strategy encourages the development, of new therapeutics for schizophrenia that move beyond positive symptoms as clinical targets to focus on dimensions of the illness most, associated with functional disability. The goal of the MATRICS initiative is to address important, obstacles that are likely to interfere with the development of new pharmacological approaches to improving neurocognition in schizophrenia.