ReviewSchizophrenia research2026
Therapeutic potential of metabotropic glutamate receptor 7 modulation in correcting cognitive deficits of schizophrenia.
Review in Schizophrenia research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Cognitive deficits in schizophrenia are a major predictor of patient functional outcome, and current treatments have limited efficacy in targeting this symptom domain. Glutamatergic dysfunction is hypothesized to contribute to cognitive impairments, and administration of N-methyl-d-aspartate (NMDA) receptor antagonists to both healthy humans and animals causes behavioral and cognitive deficits similar to those observed in patients with schizophrenia. In particular, hypofunction of NMDA receptors on GABAergic interneurons in the medial prefrontal cortex (mPFC) leads to excessive pyramidal cell activity and is a hypothesized mechanism underlying these deficits. As such, therapeutic modulation of glutamatergic and GABAergic release in PFC-associated circuits may correct cognitive impairments in schizophrenia. Metabotropic glutamate (mGlu) receptors have emerged as a promising strategy to target this symptom domain due to their widespread expression in relevant brain regions and their implications within the glutamate system. Group III mGlu receptors (mGlu
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