The genetic lexicon of dyslexia

被引:107
|
作者
Paracchini, Silvia [1 ]
Scerri, Thomas [1 ]
Monaco, Anthony P. [1 ]
机构
[1] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England
基金
英国惠康基金;
关键词
reading disability; association studies; gene expression; epistasis; cognition; neuronal migration; QUANTITATIVE-TRAIT LOCUS; DEFICIT HYPERACTIVITY DISORDER; PHONOLOGICAL CODING DYSLEXIA; FAMILY-BASED ASSOCIATION; DEVELOPMENTAL DYSLEXIA; READING-DISABILITY; NEURONAL MIGRATION; CHROMOSOME; 6P; TETRATRICOPEPTIDE REPEAT; LANGUAGE IMPAIRMENT;
D O I
10.1146/annurev.genom.8.080706.092312
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Reading abilities are acquired only through specific teaching and training. A significant proportion of children fail to achieve these skills despite normal intellectual abilities and an appropriate opportunity to learn. Difficulty in learning to read is attributable to specific dysfunctions of the brain, which so far remain poorly understood. However, it is recognized that the neurological basis for dyslexia, or reading disability, is caused in large part by genetic factors. Linkage studies have successfully identified several regions of the human genome that are likely to harbor susceptibility genes for dyslexia. In the past few years there have been exciting advances with the identification of four candidate genes located within three of these linked chromosome regions: DYX1C1 on chromosome 15, ROBO1 on chromosome 3, and KIAA0319 and DCDC2 on chromosome 6. Functional studies of these genes are offering new insights about the biological mechanisms underlying the development of dyslexia and, in general, of cognition.
引用
收藏
页码:57 / 79
页数:23
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