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      Rethinking Social Cognition in Light of Psychosis: Reciprocal Implications for Cognition and Psychopathology

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          Abstract

          The positive symptoms of psychosis largely involve the experience of illusory social actors, and yet our current measures of social cognition, at best, only weakly predict their presence. We review evidence to suggest that the range of current approaches in social cognition is not sufficient to explain the fundamentally social nature of these experiences. We argue that social agent representation is an important organizing principle for understanding social cognition and that alterations in social agent representation may be a factor in the formation of delusions and hallucination in psychosis. We evaluate the feasibility of this approach in light of clinical and nonclinical studies, developmental research, cognitive anthropology, and comparative psychology. We conclude with recommendations for empirical testing of specific hypotheses and how studies of social cognition could more fully capture the extent of social reasoning and experience in both psychosis and more prosaic mental states.

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          Most cited references108

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          Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia.

          The clinical hallmark of schizophrenia is psychosis. The objective of this overview is to link the neurobiology (brain), the phenomenological experience (mind), and pharmacological aspects of psychosis-in-schizophrenia into a unitary framework. Current ideas regarding the neurobiology and phenomenology of psychosis and schizophrenia, the role of dopamine, and the mechanism of action of antipsychotic medication were integrated to develop this framework. A central role of dopamine is to mediate the "salience" of environmental events and internal representations. It is proposed that a dysregulated, hyperdopaminergic state, at a "brain" level of description and analysis, leads to an aberrant assignment of salience to the elements of one's experience, at a "mind" level. Delusions are a cognitive effort by the patient to make sense of these aberrantly salient experiences, whereas hallucinations reflect a direct experience of the aberrant salience of internal representations. Antipsychotics "dampen the salience" of these abnormal experiences and by doing so permit the resolution of symptoms. The antipsychotics do not erase the symptoms but provide the platform for a process of psychological resolution. However, if antipsychotic treatment is stopped, the dysregulated neurochemistry returns, the dormant ideas and experiences become reinvested with aberrant salience, and a relapse occurs. The article provides a heuristic framework for linking the psychological and biological in psychosis. Predictions of this hypothesis, particularly regarding the possibility of synergy between psychological and pharmacological therapies, are presented. The author describes how the hypothesis is complementary to other ideas about psychosis and also discusses its limitations.
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            Is adolescence a sensitive period for sociocultural processing?

            Adolescence is a period of formative biological and social transition. Social cognitive processes involved in navigating increasingly complex and intimate relationships continue to develop throughout adolescence. Here, we describe the functional and structural changes occurring in the brain during this period of life and how they relate to navigating the social environment. Areas of the social brain undergo both structural changes and functional reorganization during the second decade of life, possibly reflecting a sensitive period for adapting to one's social environment. The changes in social environment that occur during adolescence might interact with increasing executive functions and heightened social sensitivity to influence a number of adolescent behaviors. We discuss the importance of considering the social environment and social rewards in research on adolescent cognition and behavior. Finally, we speculate about the potential implications of this research for society.
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              Social cognition in schizophrenia.

              Individuals with schizophrenia exhibit impaired social cognition, which manifests as difficulties in identifying emotions, feeing connected to others, inferring people's thoughts and reacting emotionally to others. These social cognitive impairments interfere with social connections and are strong determinants of the degree of impaired daily functioning in such individuals. Here, we review recent findings from the fields of social cognition and social neuroscience and identify the social processes that are impaired in schizophrenia. We also consider empathy as an example of a complex social cognitive function that integrates several social processes and is impaired in schizophrenia. This information may guide interventions to improve social cognition in patients with this disorder.
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                Author and article information

                Journal
                Clin Psychol Sci
                Clin Psychol Sci
                CPX
                spcpx
                Clinical Psychological Science
                SAGE Publications (Sage CA: Los Angeles, CA )
                2167-7026
                2167-7034
                10 February 2017
                May 2017
                : 5
                : 3
                : 537-550
                Affiliations
                [1 ]Division of Psychiatry, University College London
                [2 ]Institute of Cognitive Neuroscience, University College London
                [3 ]Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience, King’s College London
                [4 ]Department of Philosophy, Durham University
                Author notes
                [*]Vaughan Bell, Division of Psychiatry, University College London, 6th Floor, Maple House, 149 Tottenham Court Road, London W1T 7NF, United Kingdom. E-mail: Vaughan.Bell@ 123456ucl.ac.uk

                Author Contributions: V. Bell drafted the initial version of the paper. K. L. Mills., G. Modinos, and S. Wilkinson contributed additional text and provided critical revisions. All authors approved the final version for submission.

                Article
                10.1177_2167702616677079
                10.1177/2167702616677079
                5437982
                28533946
                d5505de4-327b-422a-8255-83a4ad8211e1
                © The Author(s) 2017

                This article is distributed under the terms of the Creative Commons Attribution 4.0 License ( http://www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 19 August 2016
                : 9 October 2016
                Funding
                Funded by: Wellcome Trust, FundRef http://dx.doi.org/10.13039/100004440;
                Award ID: 091667
                Funded by: Wellcome Trust, FundRef http://dx.doi.org/10.13039/100004440;
                Award ID: WT098455MA
                Funded by: Wellcome Trust, FundRef http://dx.doi.org/10.13039/100004440;
                Award ID: 200589/Z/16/Z
                Funded by: UCL-NIH Graduate Partnership Program, ;
                Funded by: King’s College London Prize Fellowship, ;
                Categories
                Theoretical/Methodological/Review Articles

                psychosis,social cognition,delusion,hallucination,schizophrenia

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