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Nuclear receptor NR4A2 IVS6 +18insG and brain derived neurotrophic factor ( BDNF ) V66M polymorphisms and risk of Taiwanese parkinson's disease
Author(s) -
Chen ChiungMei,
Chen ICheng,
Chang KuoHsuan,
Chen YiChun,
Lyu RongKuo,
Liu YenTzu,
Hu FenJu,
Chao ChihYing,
LeeChen GueyJen,
Wu YihRu
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.30476
Subject(s) - neurotrophic factors , dopaminergic , parkinson's disease , brain derived neurotrophic factor , nuclear receptor , medicine , neurotrophin , genotype , biology , endocrinology , disease , neurogenesis , neuroscience , dopamine , genetics , receptor , gene , transcription factor
Both of environmental and genetic factors confer vulnerability to Parkinson's disease (PD). NR4A2 (Nurr1), a member of the steroid/thyroid hormone nuclear receptor superfamily, is essential for the neurogenesis and differentiation of dopaminergic neurons in the midbrain. Brain derived neurotrophic factor (BDNF) deficiency may play a role in the pathogenesis of PD, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF. This study examines whether BDNF V66M (c.196 G → A) or NR4A2 IVS6 +18insG polymorphism is associated with the risk of Taiwanese PD and the age of onset using a case‐control study. The genotype or allele frequency distribution of both BDNF V66M and NR4A2 IVS6 +18insG polymorphisms was not significantly different between the cases and the controls. Neither BDNF nor NR4A2 polymorphism influences PD onset age. Notably, after stratification by sex, female individuals carrying the NR4A2 2G/2G genotype demonstrated a trend toward significant decrease in risk of developing PD (OR = 0.49, 95% CI = 0.25–0.96, P = 0.039). These results suggest that the NR4A2 IVS6 +18insG polymorphism may play a minor role in PD susceptibility among Taiwanese women. © 2007 Wiley‐Liss, Inc.