期刊
MOLECULAR PSYCHIATRY
卷 16, 期 1, 页码 97-107出版社
SPRINGERNATURE
DOI: 10.1038/mp.2009.102
关键词
mismatch negativity; expression; glucose transporter; dyslexia; speech perception
资金
- Deutsche Forschungsgemeinschaft
- EU [018696]
- Alfried Krupp von Bohlen und Halbach-Stiftung
Dyslexia is one of the most common learning disorders affecting about 5% of all school-aged children. It has been shown that event-related potential measurements reveal differences between dyslexic children and age-matched controls. This holds particularly true for mismatch negativity (MMN), which reflects automatic speech deviance processing and is altered in dyslexic children. We performed a whole-genome association analysis in 200 dyslexic children, focusing on MMN measurements. We identified rs4234898, a marker located on chromosome 4q32.1, to be significantly associated with the late MMN component. This association could be replicated in an independent second sample of 186 dyslexic children, reaching genome-wide significance in the combined sample (P = 5.14e-08). We also found an association between the late MMN component and a two-marker haplotype of rs4234898 and rs11100040, one of its neighboring single nucleotide polymorphisms (SNPs). In the combined sample, this marker combination withstands correction for multiple testing (P = 6.71e-08). Both SNPs lie in a region devoid of any protein-coding genes; however, they both show significant association with mRNA-expression levels of SLC2A3 on chromosome 12, the predominant facilitative glucose transporter in neurons. Our results suggest a possible transregulation effect on SLC2A3, which might lead to glucose deficits in dyslexic children and could explain their attenuated MMN in passive listening tasks. Molecular Psychiatry (2011) 16, 97-107; doi:10.1038/mp.2009.102; published online 29 September 2009
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