Association of body mass index-related single nucleotide polymorphisms with psychiatric disease and memory performance in a Japanese population

2016 ◽  
Vol 29 (5) ◽  
pp. 299-308 ◽  
Author(s):  
Midori Ninomiya-Baba ◽  
Junko Matsuo ◽  
Daimei Sasayama ◽  
Hiroaki Hori ◽  
Toshiya Teraishi ◽  
...  

ObjectiveObesity is a risk factor for psychiatric diseases. Recently, a number of single nucleotide polymorphisms (SNPs) have been shown to be related to body mass index (BMI). In this study, we investigated the association of BMI-related SNPs with psychiatric diseases and one of their endophenotypes, memory performance, in a Japanese population.MethodsThe subjects were 1624 patients with one of three psychiatric diseases (799 patients with major depressive disorder, 594 with schizophrenia, and 231 with bipolar disorder) and 1189 healthy controls. Memory performance was assessed using the Wechsler Memory Scale – Revised (WMS-R). Genomic DNA was prepared from venous blood and used to genotype 23 BMI-related SNPs using the TaqMan 5′-exonuclease allelic discrimination assay. We then analysed the relationships between the SNPs and psychiatric disease and various subscales of the WMS-R.ResultsThree SNPs (rs11142387, rs12597579, and rs6548238) showed significant differences in the genotype or allele frequency between patients with any psychiatric diseases and controls. Furthermore, six SNPs (rs11142387, rs12597579, rs2815752, rs2074356, rs4776970, and rs2287019) showed significant differences in at least one subscale of the WMS-R depending on the genotypes of the healthy controls. Interestingly, rs11142387 near the Kruppel-like factor 9 (KLF9) was significantly associated with psychiatric disease and poor memory function.ConclusionsWe identified three and six BMI-related SNPs associated with psychiatric disease and memory performance, respectively. In particular, carrying the A allele of rs11142387 near KLF9 was found to be associated with psychiatric disease and poor memory performance, which warrants further investigations.

2003 ◽  
Vol 18 (6) ◽  
pp. 413-418 ◽  
Author(s):  
Shinobu Ikeda ◽  
Kouichi Kurose ◽  
Shogo Ozawa ◽  
Kimie Sai ◽  
Ryuichi Hasegawa ◽  
...  

Author(s):  
Nóra Török ◽  
Rita Maszlag-Török ◽  
Kinga Molnár ◽  
Zoltán Szolnoki ◽  
Ferenc Somogyvári ◽  
...  

Earlier studies reported alterations of the kynurenine (KYN) pathway of tryptophan (TRP) metabolism in Parkinson’s disease (PD). The first rate-limiting enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan dioxygenase were observed upregulated, resulting elevated KYN/TRP ratios in the serum and cerebrospinal fluid samples of patients with PD. An increasing number of single nucleotide polymorphisms (SNPs) have been identified in a population of PD. However, little is known if genetic variations of the IDO contribute to disturbance of the KYN metabolism in and the pathogenesis of PD. SNP analysis of IDO1 was performed by allelic discrimination assay with fluorescently labelled TaqMan probes and a subgroup analysis was conducted according to the age of PD onset. The frame shifts variant rs34155785, intronic variant rs7820268, and promotor region variant rs9657182 SNPs of 105 PD patients without comorbidity were analyzed and compared to 129 healthy controls. No significant correlation was found in three SNPs between PD patients and healthy controls. However, the subgroup analysis revealed that A alleles of rs7820268 SNP or rs9657182 SNP carriers contribute to later onset of PD than non-carriers. The study suggested that SNPs of IDO1 influenced the age onset of PD and genotyping of SNPs in certain alleles potentially serves as a risk biomarker of PD.


2009 ◽  
Vol 27 (5) ◽  
pp. 323-327 ◽  
Author(s):  
Reiko Iida ◽  
Misuzu Ueki ◽  
Haruo Takeshita ◽  
Junko Fujihara ◽  
Tamiko Nakajima ◽  
...  

2001 ◽  
Vol 2 (2) ◽  
pp. 117-118 ◽  
Author(s):  
A Hirano ◽  
H Nagai ◽  
H Harada ◽  
S Haga ◽  
T Kajiwara ◽  
...  

Author(s):  
А.С. Москалев ◽  
Ф.В. Подольский ◽  
С.М. Зайцев ◽  
Е.А. Новикова ◽  
А.В. Полоников ◽  
...  

В исследование были включены 256 пациентов с колоректальным раком (134 мужчины, 122 женщины) и 608 практически здоровых добровольцев (279 мужчин, 329 женщин). Генотипирование однонуклеотидных полиморфизмов I462V (rs1048943) CYP1A1, -154A>C (rs762551) CYP1A2 и L432V (rs1056836) CYP1B1 было проведено методом ПЦР в режиме реального времени. Полиморфизм rs1056836 CYP1B1 (замена L432V) ассоциировался с повышенным риском колоректального рака в популяции Центральной России: OR=1,48, 95%CI=1,07-2,04; р=0,02. A total of 256 patients with colorectal cancer (134 males, 122 females) and 608 age- and sex-matched healthy controls (279 males, 329 females) were recruited for the study. Genotyping of single nucleotide polymorphisms (SNPs) I462V (rs1048943) CYP1A1, -154A>C (rs762551) CYP1A2 and L432V (rs1056836) CYP1B1 were done using Taq-Man-based assays. Polymorphism rs1056836 (substitution L432V) CYP1B1 was associated with increased risk of colorectal cancer in the population from Central Russia: OR=1,48, 95%CI=1,07-2,04; p=0,02.


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