Deterioration in cognitive control related mPFC function underlying development of treatment resistance in early psychosis.

Journal article

Crisp, C., Sahni, Angad, Pang, Sze W, Vanes, Lucy D, Szentgyorgyi, Timea, Averbeck, B., Moran, Rosalyn J and Shergill, Sukhwinder S 2024. Deterioration in cognitive control related mPFC function underlying development of treatment resistance in early psychosis. Scientific Reports. 14 (1), p. 12985. https://doi.org/10.1038/s41598-024-63474-1
AuthorsCrisp, C., Sahni, Angad, Pang, Sze W, Vanes, Lucy D, Szentgyorgyi, Timea, Averbeck, B., Moran, Rosalyn J and Shergill, Sukhwinder S
AbstractOne third of people with psychosis become antipsychotic treatment-resistant and the underlying mechanisms remain unclear. We investigated whether altered cognitive control function is a factor underlying development of treatment resistance. We studied 50 people with early psychosis at a baseline visit (mean < 2 years illness duration) and follow-up visit (1 year later), when 35 were categorized at treatment-responsive and 15 as treatment-resistant. Participants completed an emotion-yoked reward learning task that requires cognitive control whilst undergoing fMRI and MR spectroscopy to measure glutamate levels from Anterior Cingulate Cortex (ACC). Changes in cognitive control related activity (in prefrontal cortex and ACC) over time were compared between treatment-resistant and treatment-responsive groups and related to glutamate. Compared to treatment-responsive, treatment-resistant participants showed blunted activity in right amygdala (decision phase) and left pallidum (feedback phase) at baseline which increased over time and was accompanied by a decrease in medial Prefrontal Cortex (mPFC) activity (feedback phase) over time. Treatment-responsive participants showed a negative relationship between mPFC activity and glutamate levels at follow-up, no such relationship existed in treatment-resistant participants. Reduced activity in right amygdala and left pallidum at baseline was predictive of treatment resistance at follow-up (67% sensitivity, 94% specificity). The findings suggest that deterioration in mPFC function over time, a key cognitive control region needed to compensate for an initial dysfunction within a social-emotional network, is a factor underlying development of treatment resistance in early psychosis. An uncoupling between glutamate and cognitive control related mPFC function requires further investigation that may present a future target for interventions. [Abstract copyright: © 2024. The Author(s).]
KeywordsCognitive control; Magnetic Resonance Imaging; Cognition; Glutamate; Male; Female; Young Adult; Gyrus Cinguli - metabolism - diagnostic imaging - physiopathology; Schizophrenia; Spectroscopy; Humans; Psychotic Disorders - metabolism - drug therapy - physiopathology; Prefrontal Cortex - metabolism - physiopathology - diagnostic imaging; Adult; Glutamic Acid - metabolism; fMRI; Treatment resistance; Antipsychotic Agents - therapeutic use - pharmacology
Year2024
JournalScientific Reports
Journal citation14 (1), p. 12985
PublisherSpringer Nature
ISSN2045-2322
Digital Object Identifier (DOI)https://doi.org/10.1038/s41598-024-63474-1
Official URLhttps://www.nature.com/articles/s41598-024-63474-1
Publication dates
Online06 Jun 2024
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Deposited19 Jun 2024
Accepted29 May 2024
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