Upregulation ofneuroinflammation and arachidonic acid cascade markers andloss of synaptic markers in frontal cortex from schizophrenic patients

Schizophrenia (SZ) is a severe, debilitating and progressive psychiatric disorder, associated with cognitive decline. An increased arachidonic acid (AA) cascade signaling associated with upregulated neuroinflammation and along with increased synaptic loss is common to Alzheimers pathology. On this basis, we tested the hypothesis that SZ pathology is associated with increased AA cascade and neuroinflammatory markers and with synaptic loss. To do this, we used western blotting and RT‐PCR to compare protein and mRNA levels of AA cascade markers, neuroinflammatory and synaptic markers in postmortem frontal cortex from 10 SZ patients and 10 matched controls. Mean protein and mRNA levels of cytosolic and secretory phospholipase A 2 (cPLA 2 type IVA, sPLA 2 type IIA) and cyclooxygenase (COX)‐2, were significantly elevated in postmortem brain tissue from BD and SZ patients. Whereas, protein and mRNA levels of interleukin‐1beta, glial protein acidic protein and Cd11b were significantly increased in the SZ. In addition, reduced synaptophysin and drebrin were found in postmortem frontal cortex from SZ patients. Increased neuroinflammation with upregulated AA cascade enzymes might lead to disease progression and cognitive defects in SZ patients. Downregulation of this cascade might thus be considered for developing new therapies.