Abstract
The N-methyl-d-aspartate receptor (NMDAR) hypofunction model of schizophrenia suggests that dysfunction of these receptors leads to an excess release of glutamate and could explain the brain structural abnormalities characterizing these patients. In NMDAR encephalitis (NMDARE), which holds clinical similarities with schizophrenia, autoantibodies target NMDARs, leading to increased levels of glutamatergic metabolites in brain tissue. No study so far has examined these disorders comparatively.
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