Fig. 5. Expression of NF-κB transcripts in the postmortem DLPFC of schizophrenia patients with neuroinflammation relative to non-schizophrenic controls with neuroinflammation.

A Not all patients show evidence of neuroinflammation (red = proportion of ‘inflamed’ patients, grey = non-inflamed patients), and some individuals without schizophrenia do show evidence of neuroinflammation (blue = ‘inflamed’ controls, grey = non-inflamed controls). Comparing cortical mRNA levels of NF-κB pathway members between high inflammation patients and high inflammation controls allows for identification of schizophrenia-specific abnormalities in this critical immunomodulatory pathway. B Such comparisons have shown that high neuroinflammation patients may actually have ‘blunted’ NF-κB activation, which may represent cell-specific deficits and/or a failure to adequately induce NF-κB to the level required to initiate NF-κB-dependent anti-inflammatory processes in the brain.