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Family‐based and case‐control studies reveal no association of lipocalin‐type prostaglandin D2 synthase with schizophrenia
Author(s) -
Ruano Dina,
Macedo António,
Soares Maria João,
Valente José,
Azevedo Maria Helena,
Pato Carlos,
Hutz Mara Helena,
Gama Clarissa S.,
Lobato Maria Inês,
BelmontedeAbreu Paulo,
Heutink Peter,
Palha Joana Almeida
Publication year - 2007
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30477
Subject(s) - prostaglandin d2 , schizophrenia (object oriented programming) , biology , lipocalin , prostaglandin , medicine , endocrinology , genetics , psychiatry
Several observations point to the involvement of disturbed lipid biology in schizophrenia. Reduced response to niacin flushing test, which involves vasodilatation induced by prostaglandin D2 (PGD2), is among the evidences, together with decreased CSF levels of lipocalin‐type prostaglandin D2 synthase (PTGDS), the enzyme responsible for the synthesis of PGD2 in the brain. Since PTGDS is also a carrier for lipophilic molecules such as retinoids and thyroid hormones, altered PTGDS levels might influence both PGD2‐mediated signaling, and vitamin A and thyroid hormone availability. To test whether genetic variants of PTGDS are involved in the etiology of schizophrenia, we searched for variants in the coding and regulatory regions of the gene. We identified four previously described polymorphisms. Using two case‐control samples from Portugal and Brazil, none of the polymorphisms tested was associated with the disease. In addition, no transmission distortion was observed in an independent parents‐offspring sample from the Azorean Islands. Our data do not support the involvement of the PTGDS gene in the etiology of schizophrenia. © 2007 Wiley‐Liss, Inc.