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Mapping the pathophysiology of schizophrenia: interactions between multiple cellular pathways

Journal Article


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Abstract


  • Schizophrenia is a complex disorder involving dysregulation of multiple pathways in its pathophysiology. Dopaminergic, glutamatergic and GABAergic neurotransmitter systems are affected in schizophrenia and interactions between these receptors contribute to the pathophysiology of the disease. Deficits in acetylcholine muscarinic receptors have been identified in a sub-group of individuals with schizophrenia. Inflammation has also been found to play a major role in the development and exacerbation of psychotic symptoms in schizophrenia. Additionally, evidence from genetic, post-mortem and animal studies over the past decade has identified a number of susceptibility factors for schizophrenia, including neuregulin 1 (Nrg1) and its receptor ErbB4, disrupted-in-schizophrenia-1 (DISK1), dysbindin-1, catechol-O-methyl tranferase (COMT), BDNF, and Akt. These factors and related pathways interact closely with dopaminergic, glutamatergic and GABAergic neurotransmitter systems. A key question is how do these interactions contribute to the pathophysiology of schizophrenia? More specifically, how do these components interact during early brain development based on the view of schizophrenia as a developmental disorder? Therefore, this special issue aims to map the pathophysiology of schizophrenia by illuminating the interactive nature of specific pathways on different levels of the brain from cellular pathways and neural circuits to functional deficits.

Authors


Publication Date


  • 2013

Citation


  • Deng, C. & Dean, B. (2013). Mapping the pathophysiology of schizophrenia: interactions between multiple cellular pathways. Frontiers in Cellular Neuroscience, 7 (1), 238-1-238-2.

Scopus Eid


  • 2-s2.0-84908621871

Ro Full-text Url


  • http://ro.uow.edu.au/cgi/viewcontent.cgi?article=1400&context=ihmri

Ro Metadata Url


  • http://ro.uow.edu.au/ihmri/383

Has Global Citation Frequency


Start Page


  • 238-1

End Page


  • 238-2

Volume


  • 7

Issue


  • 1

Place Of Publication


  • Switzerland

Abstract


  • Schizophrenia is a complex disorder involving dysregulation of multiple pathways in its pathophysiology. Dopaminergic, glutamatergic and GABAergic neurotransmitter systems are affected in schizophrenia and interactions between these receptors contribute to the pathophysiology of the disease. Deficits in acetylcholine muscarinic receptors have been identified in a sub-group of individuals with schizophrenia. Inflammation has also been found to play a major role in the development and exacerbation of psychotic symptoms in schizophrenia. Additionally, evidence from genetic, post-mortem and animal studies over the past decade has identified a number of susceptibility factors for schizophrenia, including neuregulin 1 (Nrg1) and its receptor ErbB4, disrupted-in-schizophrenia-1 (DISK1), dysbindin-1, catechol-O-methyl tranferase (COMT), BDNF, and Akt. These factors and related pathways interact closely with dopaminergic, glutamatergic and GABAergic neurotransmitter systems. A key question is how do these interactions contribute to the pathophysiology of schizophrenia? More specifically, how do these components interact during early brain development based on the view of schizophrenia as a developmental disorder? Therefore, this special issue aims to map the pathophysiology of schizophrenia by illuminating the interactive nature of specific pathways on different levels of the brain from cellular pathways and neural circuits to functional deficits.

Authors


Publication Date


  • 2013

Citation


  • Deng, C. & Dean, B. (2013). Mapping the pathophysiology of schizophrenia: interactions between multiple cellular pathways. Frontiers in Cellular Neuroscience, 7 (1), 238-1-238-2.

Scopus Eid


  • 2-s2.0-84908621871

Ro Full-text Url


  • http://ro.uow.edu.au/cgi/viewcontent.cgi?article=1400&context=ihmri

Ro Metadata Url


  • http://ro.uow.edu.au/ihmri/383

Has Global Citation Frequency


Start Page


  • 238-1

End Page


  • 238-2

Volume


  • 7

Issue


  • 1

Place Of Publication


  • Switzerland