The intergenerational multiple deficit model and the case of dyslexia

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)...

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Bibliographic Details
Published in:Frontiers in human neuroscience 2014-06, Vol.8, p.346-346
Main Authors: van Bergen, Elsje, van der Leij, Aryan, de Jong, Peter F
Format: Article
Language:English
Subjects:
Attention deficit hyperactivity disorder
Children
Children & youth
Comorbidity
developmental disorders
Dyslexia
Etiology
Families & family life
generalist genes hypothesis
Hyperactivity
Hypotheses
intergenerational multiple deficit model
intergenerational transmission
Liability
Literacy
Longitudinal studies
Neuroscience
Phonology
Reading comprehension
Risk factors
Sound
Studies
Twins
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Summary: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.
ISSN:1662-5161
1662-5161
DOI:10.3389/fnhum.2014.00346