Harry Pantazopoulos

TL;DR: Marked changes in functionally relevant molecules in schizophrenia point to a pivotal role for extracellular matrix-glial interactions in the pathogenesis of this disease.

TL;DR: The study provides strong evidence for a specific defect of hippocampus interneurons in schizophrenia and has implications for emerging models of hippocampal dysfunction in schizophrenia.

TL;DR: These findings suggest that PNN deficit contributes to PFC dysfunction in schizophrenia, and that the timing of PNN development overlaps with the period when schizophrenia symptomatology gradually emerges raises the possibility that aberrant PNN formation might contribute to the onset of illness.

TL;DR: The findings raise the possibility that the infralimbic cortex inhibits conditioned fear via the excitation of intercalated cells and the consequent inhibition of central amygdala neurons.

TL;DR: Evidence for PNN abnormalities in schizophrenia, the potential functional impact of such abnormalities on inhibitory circuits and, in turn, cognitive and emotion processing are discussed, and the physiological process of PNN remodeling may be disrupted in schizophrenia as a result of interactions between matrix remodeling processes and immune system dysregulation are speculated.