Abstract
Which children go on to develop dyslexia? Since dyslexia has a multifactorial etiology, this question can be restated as: what are the factors that put children at high risk for developing dyslexia? It is argued that a useful theoretical framework to address this question is Pennington’s (2006) multiple deficit model (MDM). This model replaces models that attribute dyslexia to a single underlying cause. Subsequently, the generalist genes hypothesis for learning (dis)abilities (Plomin and Kovas, 2005) is described and integrated with the MDM. Next, findings are presented from a longitudinal study with children at family risk for dyslexia. Such studies can contribute to testing and specifying the MDM. In this study, risk factors at both the child and family level were investigated. This led to the proposed intergenerational MDM, in which both parents confer liability via intertwined genetic and environmental pathways. Future scientific directions are discussed to investigate parent-offspring resemblance and transmission patterns, which will shed new light on disorder etiology.
Highlights
TESTING THE multiple deficit model (MDM) We argue here that a line of inquiry that can contribute to testing and specifying the MDM are family risk studies
As genetic screening of children for their dyslexia susceptibility is still far away, we propose an indicator of their genetic risk
The MDM predicts that some of the cognitive processes related to dyslexia are specific to dyslexia and others are shared with comorbid neurodevelopmental disorders
Summary
The MDM predicts that some of the cognitive processes related to dyslexia are specific to dyslexia (or reading ability in general) and others are shared with comorbid neurodevelopmental disorders (and their accompanying continuous phenotype). Our findings are in agreement with findings from other family risk studies, which failed to show effects of home literacy environment on children’s reading outcome (Elbro et al, 1998; Snowling et al, 2007; Torppa et al, 2007; van Bergen et al, 2011).
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