Martin, Andrew K., Robinson, G., Dzafic, I., Reutens, D., Mowry, B. (2014) Theory of mind and the social brain: Implications for understanding the genetic basis of schizophrenia. Genes, Brain and Behavior, 13 (1). pp. 104-117. ISSN 1601-1848. (doi:10.1111/gbb.12066) (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided) (KAR id:79714)
The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided. | |
Official URL: https://doi.org/10.1111/gbb.12066 |
Abstract
Genome-wide association studies in schizophrenia have recently made significant progress in our understanding of the complex genetic architecture of this disorder. Many genetic loci have been identified and now require functional investigation. One approach involves studying their correlation with neuroimaging and neurocognitive endophenotypes. Theory of Mind (ToM) deficits are well established in schizophrenia and they appear to fulfill criteria for being considered an endophenotype. We aim to review the behavioral and neuroimaging-based studies of ToM in schizophrenia, assess its suitability as an endophenotype, discuss current findings, and propose future research directions. Suitable research articles were sourced from a comprehensive literature search and from references identified through other studies. ToM deficits are repeatable, stable, and heritable: First-episode patients, those in remission and unaffected relatives all show deficits. Activation and structural differences in brain regions believed important for ToM are also consistently reported in schizophrenia patients at all stages of illness, although no research to date has examined unaffected relatives. Studies using ToM as an endophenotype are providing interesting genetic associations with both single nucleotide polymorphisms (SNPs) and specific copy number variations (CNVs) such as the 22q11.2 deletion syndrome. We conclude that ToM is an important cognitive endophenotype for consideration in future studies addressing the complex genetic architecture of schizophrenia, and may help identify more homogeneous clinical sub-types for further study.
Item Type: | Article |
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DOI/Identification number: | 10.1111/gbb.12066 |
Uncontrolled keywords: | allele; article; brain region; cell activation; chromosome 22q; cognitive defect; copy number variation; endophenotype; executive function; functional magnetic resonance imaging; gene locus; genetic association; human; nerve cell; priority journal; schizophrenia; single nucleotide polymorphism; social interaction; theory of mind, 22q deletion syndrome, ZNF804A; Behavior; COMT; copy number variants; DAOA; endophenotype; genetics; mutations, neurexin; neuroimaging; OXTR, phenotype; psychiatry; schizophrenia; single nucleotide polymorphisms; social cognition; theory of mind, Brain; Genome, Human; Humans; Phenotype; Polymorphism, Genetic; Schizophrenia; Social Behavior; Theory of Mind |
Divisions: | Divisions > Division of Human and Social Sciences > School of Psychology |
Depositing User: | Andrew Martin |
Date Deposited: | 05 Feb 2020 10:20 UTC |
Last Modified: | 06 Mar 2023 12:31 UTC |
Resource URI: | https://kar.kent.ac.uk/id/eprint/79714 (The current URI for this page, for reference purposes) |
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