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No association between BDNF Val66Met polymorphism and emergence of psychiatric symptoms in systemic lupus erythematosus patients
Author(s) -
IkenouchiSugita Atsuko,
Yoshimura Reiji,
Kishi Taro,
UmeneNakano Wakako,
Hori Hikaru,
Katsuki Asuka,
Saito Kazuyoshi,
Iwata Nakao,
Tanaka Yoshiya,
Nakamura Jun
Publication year - 2011
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.1203
Subject(s) - brain derived neurotrophic factor , genotyping , medicine , neurotrophic factors , pathogenesis , neurotransmitter , allele , polymorphism (computer science) , endocrinology , immunology , psychiatry , genotype , gene , central nervous system , biology , receptor , genetics
Background Brain‐derived neurotrophic factor (BDNF) plays an important role in the regulation of synaptic plasticity and neurotransmitter release across multiple neurotransmitter systems. Recent studies have suggested that BDNF plays a role in the pathogenesis of psychiatric symptoms in patients with systemic lupus erythematosus (SLE). Objectives We hypothesized that the polymorphism of BDNF Val66Met is associated with the emergence of psychiatric symptoms (PS) and serum BDNF levels in SLE patients. To examine the hypothesis, we compared the BDNF Val66Met polymorphism and serum BDNF levels in patients with SLE with or without PS. Methods Psychiatric symptoms were assessed in 54 patients with SLE. PS were evaluated using the Brief Psychiatric Rating Scale. Genotyping was carried out using a 54‐nuclease assay. Serum BDNF levels were measured by using enzyme‐linked immunosorbent assay. Results The presence of the Met allele was not significantly associated with the presence of PS or with serum BDNF levels in patients with SLE. Conclusion Our data do not support the common variant Val66Met of the BDNF gene as an etiologic factor in the various forms of PS and serum BDNF levels in SLE. Copyright © 2011 John Wiley & Sons, Ltd.