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Cortical GABA In Subjects At Ultra-High Risk Of Psychosis: Relationship To Negative Prodromal Symptoms

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Gemma Modinos, Fatma Simsek, Jamie Horder, Matthijs Geert Bossong, Ilaria Bonoldi, Matilda Azis, Jesus Perez, Matthew Broome, David John Lythgoe, James Michael Stone, Oliver David Howes, Declan G Murphy, Anthony A Grace, Paul Allen, Philip McGuire

Original languageEnglish
JournalInternational Journal of Neuropsychopharmacology
Published19 Aug 2017

King's Authors


Background: Whilst robust preclinical and postmortem evidence suggests that altered GABAergic function is central to the development of psychosis, little is known about whether it is altered in subjects at ultra-high risk of psychosis, or its relationship to prodromal symptoms.
Methods: Twenty-one anti-psychotic naïve UHR individuals and 20 healthy volunteers underwent proton magnetic resonance imaging at 3T. GABA levels were obtained from the medial prefrontal cortex (MPFC) using MEGA-PRESS, and expressed as peak-area ratios relative to the synchronously-acquired creatine signal. GABA levels were then related to severity of positive and negative symptoms as measured with the Community Assessment of At-Risk Mental States.
Results: Whilst we found no significant difference in GABA levels between UHR subjects and healthy controls (P = .130), in UHR individuals MPFC GABA levels were negatively correlated with the severity of negative symptoms (P = .013).
Conclusion: These findings suggest that GABAergic neurotransmission may be involved in the neurobiology of negative symptoms in the UHR state.

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