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Phospholipase A2 activity in affective bipolar disorder

Grant number: 10/07884-3
Support type:Regular Research Grants
Duration: September 01, 2010 - August 31, 2012
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Wagner Farid Gattaz
Grantee:Wagner Farid Gattaz
Home Institution: Instituto de Psiquiatria Doutor Antonio Carlos Pacheco e Silva (IPq). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Assoc. researchers: Aline Siqueira Ferreira ; Eliza Hiromi Ikenaga ; Jorge Elias Kalil Filho ; Nádia Rezende Barbosa

Abstract

The bipolar affective disorder (BAD) is one of the major psychiatric disorders. The Bipolar spectrum concept increases bipolarity rates from the conventional 1% to at least 5% of the general population. The first symptoms may manifest before 25 years of age, although in many cases they can begin between 45 and 50 years of age. According to ICD-10 and/ or DSM-IV-TR, BAD is classified into four types (I, II, III and IV). However, due to several symptomatic situations, it is not possible to prevent the progress of the disorder, in spite of the great availability of drug- related treatment. Secondary messengers are believed to play an important role in BAD. This hypothesis is based on some studies which indicated evidence for an inhibition of intracellular signal transduction resulting from phospholipase hyperactivity, which would therefore be involved in the pathophysiological mechanism of BAD. Phospholipase A2 (PLA2) comprises a superfamily of hydrolytic enzymes that cleave Ester attached to the sn-2 position of glycerophospholipis of plasmatic or subcellular membranes, resulting in arachidonic acid, a known precursor of eicosanoids, such as prostaglandins and leukotrienes. Lisophospholipedes, another lipid mediator class, were produced by the same reaction. Few studies have been performed about activities of PLA2 subtypes in mood disorders, especially BAD. Therefore, the investigation is here proposed into activities of subtypes of PLA2 (iPLA2, cPLA2 and sPLA2) in platelets of patients with BAD and healthy controls (subjects without mental disorders), seeking possible clinical and biological correlations. PLA2 may be a BAD biomarker and/or a therapeutic or preventive target. (AU)