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dc.contributor.authorJoyce, Daniel
dc.date.accessioned2023-07-26T16:14:11Z
dc.date.available2023-07-26T16:14:11Z
dc.date.issued2023-06
dc.identifier.citationElias D. Mouchlianitis, Lucy D. Vanes, Derek K. Tracy, Anne-Kathrin Fett, Daniel Joyce & Sukhi S. Shergill . Neuroimaging glutamatergic mechanisms differentiating antipsychotic treatment-response. Sci Rep 13, 8938 (2023).en
dc.identifier.urihttps://oxfordhealth-nhs.archive.knowledgearc.net/handle/123456789/1238
dc.descriptionThis is an open access article distributed under the terms of the Creative Commons CC BY license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. You are not required to obtain permission to reuse this article. To request permission for a type of use not listed, please contact Springer Natureen
dc.description.abstractGlutamatergic dysfunction is associated with failure to respond to antipsychotic medication in individuals with schizophrenia. Our objective was to combine neurochemical and functional brain imaging methods to investigate glutamatergic dysfunction and reward processing in such individuals compared with those with treatment responsive schizophrenia, and healthy controls. 60 participants played a trust task, while undergoing functional magnetic resonance imaging: 21 classified as having treatment-resistant schizophrenia, 21 patients with treatment-responsive schizophrenia, and 18 healthy controls. Proton magnetic resonance spectroscopy was also acquired to measure glutamate in the anterior cingulate cortex. Compared to controls, treatment responsive and treatment-resistant participants showed reduced investments during the trust task. For treatment-resistant individuals, glutamate levels in the anterior cingulate cortex were associated with signal decreases in the right dorsolateral prefrontal cortex when compared to those treatment-responsive, and with bilateral dorsolateral prefrontal cortex and left parietal association cortex when compared to controls. Treatment-responsive participants showed significant signal decreases in the anterior caudate compared to the other two groups. Our results provide evidence that glutamatergic differences differentiate treatment resistant and responsive schizophrenia. The differentiation of cortical and sub-cortical reward learning substrates has potential diagnostic value. Future novel interventions might therapeutically target neurotransmitters affecting the cortical substrates of the reward network.en
dc.description.urihttps://doi.org/10.1038/s41598-022-26702-0en
dc.language.isoenen
dc.subjectSchizophreniaen
dc.subjectPsychosisen
dc.subjectAntipsychoticsen
dc.titleNeuroimaging glutamatergic mechanisms differentiating antipsychotic treatment-responseen
dc.typeArticleen


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