The pathophysiology of schizophrenia has not been fully elucidated but there are converging leads to understanding
this complex psychiatric disorder. One family of molecules that may play a crucial role in the development of
schizophrenia is the eicosanoids. Review of the literature on eicosanoids in patients with schizophrenia points to findings
in three areas: precursor molecules such as polyunsaturated fatty acids (PUFAs) and specifically arachidonic acid (AA),
the actions of specific eicosanoids such as thromboxane A2 (TxA2), thromboxane B2 (TxB2) and prostaglandin E2
(PGE2), and enzymes with important functions in eicosanoid metabolism such as cyclooxygenase 2 (COX-2).
It has also been found that classical as well as second generation antipsychotics, drugs used to treat schizophrenia, influence
eicosanoid metabolism. For example, clozapine and its metabolite N-desmethylclozapine (NDMC) decreased TxB2
production in vitro.
Eicosanoids and the enzymes involved in their metabolism may provide novel future drug targets. Therapeutic response to
COX-2 inhibitors has already been demonstrated in patients at an early stage of schizophrenia. COX-2 inhibitors may exert
this therapeutic action through their effects in reducing PGE2, type-2 cytokine and kynurenic acid production and
strengthening glutamatergic neurotransmission.