Abstract
Dyslexia, a specific reading disability, is a common (up to 10% of children) and highly heritable (~70%) neurodevelopmental disorder. Behavioral and molecular genetic approaches are aimed towards dissecting its significant genetic component. In the proposed review, we will summarize advances in twin and molecular genetic research from the past 20 years. First, we will briefly outline the clinical and educational presentation and epidemiology of dyslexia. Next, we will summarize results from twin studies, followed by molecular genetic research (e.g., genome-wide association studies (GWASs)). In particular, we will highlight converging key insights from genetic research. (1) Dyslexia is a highly polygenic neurodevelopmental disorder with a complex genetic architecture. (2) Dyslexia categories share a large proportion of genetics with continuously distributed measures of reading skills, with shared genetic risks also seen across development. (3) Dyslexia genetic risks are shared with those implicated in many other neurodevelopmental disorders (e.g., developmental language disorder and dyscalculia). Finally, we will discuss the implications and future directions. As the diversity of genetic studies continues to increase through international collaborate efforts, we will highlight the challenges in advances of genetics discoveries in this field.
Highlights
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The findings showed that shared genetic effects could explain around 50% of the correlation between reading and math, a finding consistent with results from a twin-based meta-analysis [23]
While the results reported far confirm a strong polygenic nature of dyslexia, large effects associated with individual variants remain a possibility
Summary
Dyslexia is found worldwide and across languages, including transparent alphabetic orthographies, less transparent alphabetic orthographies, and logographic languages [14,15]. This school of thought requires placing an arbitrary cutoff to diagnose affected individuals (see section above on the epidemiology of dyslexia and Figure 1, including the discussion on prevalence rates based on the chosen cut point) Based on this cutoff approach, the transformation of a continuous trait of reading performance into a categorical trait, which was reflected in the methods used in twin studies in the 1990s and early 2000s (e.g., probandwise concordance and deFries–Fulker analyses), resulted, by definition, in a loss of information pertaining to the continuum of variation in reading performance. The field began to acknowledge that like essentially any other common neurodevelopmental disorder, dyslexia is heterogeneous at many levels, ranging from genetic risk factors to observable deficits across a normal distribution of reading skills These advances were, in turn, reflected in the methodology used in subsequent twin studies, with samples representing the entire population rather than only a group of individuals with dyslexia, narrowly defined by an arbitrarily set cutoff. Genetic liability for dyslexia is shared with other neurobiological learning disorders (e.g., dyscalculia) and some psychopathological disorders (e.g., internalizing)
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