31
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Cognitive Remediation in Schizophrenia

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cognitive deficits in schizophrenia are pervasive, severe, and largely independent of the positive and negative symptoms of the illness. These deficits are increasingly considered to be core features of schizophrenia with evidence that the extent of cognitive impairment is the most salient predictor of daily functioning. Unfortunately, current schizophrenia treatment has been limited in addressing the cognitive deficits of the illness. Alterations in neuroplasticity are hypothesized to underpin these cognitive deficits, though preserved neuroplasticity may offer an avenue towards cognitive remediation. Key neuroplastic principles to consider in designing remediation interventions include ensuring sufficient intensity and duration of remediation programs, "bottom-up" training that proceeds from simple to complex cognitive processes, and individual tailoring of remediation regimens. We discuss several cognitive remediation programs, including cognitive enhancement therapy, which embrace these principles to target neurocognitive and social cognitive improvements and which havebeen demonstrated to be effective in schizophrenia. Future directions in cognitive remediation research include potential synergy with pharmacologic treatment, non-invasive stimulation techniques, and psychosocial interventions, identification of patient characteristics that predict outcome with cognitive remediation, and increasing the access to these interventions in front-line settings.

          Related collections

          Most cited references105

          • Record: found
          • Abstract: found
          • Article: not found

          The MATRICS Consensus Cognitive Battery, part 1: test selection, reliability, and validity.

          The lack of an accepted standard for measuring cognitive change in schizophrenia has been a major obstacle to regulatory approval of cognition-enhancing treatments. A primary mandate of the National Institute of Mental Health's Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) initiative was to develop a consensus cognitive battery for clinical trials of cognition-enhancing treatments for schizophrenia through a broadly based scientific evaluation of measures. The MATRICS Neurocognition Committee evaluated more than 90 tests in seven cognitive domains to identify the 36 most promising measures. A separate expert panel evaluated the degree to which each test met specific selection criteria. Twenty tests were selected as a beta battery. The beta battery was administered to 176 individuals with schizophrenia and readministered to 167 of them 4 weeks later so that the 20 tests could be compared directly. The expert panel ratings are presented for the initially selected 36 tests. For the beta battery tests, data on test-retest reliability, practice effects, relationships to functional status, practicality, and tolerability are presented. Based on these data, 10 tests were selected to represent seven cognitive domains in the MATRICS Consensus Cognitive Battery. The structured consensus method was a feasible and fair mechanism for choosing candidate tests, and direct comparison of beta battery tests in a common sample allowed selection of a final consensus battery. The MATRICS Consensus Cognitive Battery is expected to be the standard tool for assessing cognitive change in clinical trials of cognition-enhancing drugs for schizophrenia. It may also aid evaluation of cognitive remediation strategies.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Synaptic plasticity: multiple forms, functions, and mechanisms.

            Experiences, whether they be learning in a classroom, a stressful event, or ingestion of a psychoactive substance, impact the brain by modifying the activity and organization of specific neural circuitry. A major mechanism by which the neural activity generated by an experience modifies brain function is via modifications of synaptic transmission; that is, synaptic plasticity. Here, we review current understanding of the mechanisms of the major forms of synaptic plasticity at excitatory synapses in the mammalian brain. We also provide examples of the possible developmental and behavioral functions of synaptic plasticity and how maladaptive synaptic plasticity may contribute to neuropsychiatric disorders.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              AMPA receptor trafficking and synaptic plasticity.

              Activity-dependent changes in synaptic function are believed to underlie the formation of memories. Two prominent examples are long-term potentiation (LTP) and long-term depression (LTD), whose mechanisms have been the subject of considerable scrutiny over the past few decades. Here we review the growing literature that supports a critical role for AMPA receptor trafficking in LTP and LTD, focusing on the roles proposed for specific AMPA receptor subunits and their interacting proteins. While much work remains to understand the molecular basis for synaptic plasticity, recent results on AMPA receptor trafficking provide a clear conceptual framework for future studies.
                Bookmark

                Author and article information

                Journal
                Clin Psychopharmacol Neurosci
                Clin Psychopharmacol Neurosci
                CPN
                Clinical Psychopharmacology and Neuroscience
                Korean College of Neuropsychopharmacology
                1738-1088
                2093-4327
                December 2012
                20 December 2012
                : 10
                : 3
                : 125-135
                Affiliations
                [1 ]Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.
                [2 ]Department of Psychiatry, Brigham and Women's Hospital, Boston, MA, USA.
                [3 ]Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
                Author notes
                Address for correspondence: Matcheri Keshavan, MD. Department of Psychiatry, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA. Tel: +1-617-754-1256, Fax: +1-617-754-1250, mkeshava@ 123456bidmc.harvard.edu
                Article
                10.9758/cpn.2012.10.3.125
                3569160
                23430145
                2240fc0c-664c-4192-bc99-5ae28577453c
                Copyright© 2012, Korean College of Neuropsychopharmacology

                This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 09 April 2012
                : 01 June 2012
                : 02 June 2012
                Categories
                Review

                schizophrenia,cognition disorders/pathology,cognition disorders/therapy,cognition disorders/rehabilitation,neuronal plasticity

                Comments

                Comment on this article