Does a monoclonal antibody targeting immune cells affect glutamatergic level in schizophrenia? A multimodal PET/MRS brain imaging study.

NeuropsychopharmacologyJul 9, 2026 (epub)
Clinical ResearchPsychiatryOpen access

Guy Hindley, Yuya Mizuno, Katherine Beck et al.

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In 30 seconds

This randomized controlled trial investigated the relationship between microglial dysfunction and glutamatergic levels in individuals with first-episode psychosis and healthy controls. The study found no significant association between anterior cingulate (ACC) glutamate levels and microglial activity, nor did treatment with the monoclonal antibody natalizumab significantly alter ACC glutamate levels (mean difference = 0.227 i.u., p = 0.139).

Key findings

  • No significant association between ACC glutamate concentration and ACC TSPO binding (β = -0.003, p = 0.55).
  • Natalizumab treatment did not significantly alter ACC glutamate levels (mean difference = 0.227 i.u., p = 0.139).
  • Study included 108 participants: 68 patients with first-episode psychosis and 40 healthy controls.

Why it matters

Understanding the mechanisms underlying glutamatergic dysregulation in schizophrenia is crucial for developing targeted therapies. This study suggests that microglial dysfunction and glutamatergic dysregulation may operate independently, which could influence future treatment strategies.

Source

Published in Neuropsychopharmacology. This summary was written by xxcode from the publication's abstract and metadata. It is not peer reviewed and is not a substitute for the original article. For clinical decisions, review the original publication.

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