Differential expression of prostaglandin D2 synthase (PTGDS) in patients with attention deficit-hyperactivity disorder and bipolar disorder

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• 作者：Juan Jesú ; s Mar&iacute ; n-Mé ; ndez^a ; ¹ ; Ana Patiñ ; o-Garc&iacute ; a^b ; ¹ ; ^{apatigar@unav.es} ; Victor Segura^c ; Felipe Ortuñ ; o^a ; Mª ; . Dolores Gá ; lvez^a ; Cé ; sar A. Soutullo^a
• 关键词：ADHD ; Bipolar disorder ; Gene expression ; Prostaglandin D2 synthase
• 刊名：Journal of Affective Disorders
• 出版年：2012
• 期刊代码：141_01650327
• 类别：med
• 出版时间：May, 2012
• 卷：138
• 期：3
• 页码：479-484
• 文件大小：437 K

摘要

Background

As marker genes for bipolar disorder (BP) and attention deficit hyperactivity disorder (ADHD) are not fully identified, we carried out a complete genome analysis to search for genes differentially expressed in ADHD and BP.

Materials and methods

We recruited 39 patients (30 ADHD, 9 BP), aged 7 to 23 years. For evaluation of the psychiatric diagnosis, we used a semi-structured interview based on the K-SADS-PL (DSM-IV). RNA was extracted from peripheral blood and analyzed with the GeneChip庐 Human Genome U133-Plus 2.0 (Affymetrix). For the validation of differentially expressed genes, real-time PCR was used.

Results

Hybridization and subsequent statistical analysis found 502 probe-sets with significant differences in expression in ADHD and BP patients. Of these, 82 had highly significant differences. Neuregulin (NRG1), cathepsins B and D (CTSB, CTSD) and prostaglandin-D2-synthase (PTGDS) were chosen for semi-quantitative mRNA determination. The expression of PTGDS was statistically increased in ADHD relative to BP patients (p = 0.01). We found no such differential expression with NRG1, CTSB and CTSD genes (p > 0.05).

Conclusions

The gene coding for PTGDS was found to be more expressed in patients with ADHD relative to patients with BP, indicating a possible link with the differential etiology of ADHD. The experimental approach we have used is, at least in part, validated by the detection of proteins directly concerned with brain functions, and shows a possible way forward for studies of the connection between brain function genes and psychiatric disorders.

Limitations

Confirmation of our findings requires a larger sample of patients with clearly-defined phenotypes.