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Neural basis for individual differences in pSTM in the normal and dyslexic populations (NBIDPSTM)
Start date: 02 Mar 2009, End date: 01 Mar 2011 PROJECT  FINISHED 

"Developmental dyslexia (DD) is a hereditary neurodevelopmental disorder, affecting 5%-10% of the population. It is associated with impoverished literacy skills despite normal intelligence and adequate educational opportunities, and occurs in the absence of major sensory impairments. There is currently much interest in the proposal that dyslexia is best characterised as a language-specific deficit in which literacy problems stem from impairment in the representation and processing of phonemes. However, a growing body of empirical evidence fails to support this view. The research proposed here tests an alternative theoretical stance, namely that deficits in phonological short-term memory (pSTM) are central to the literacy problems observed in DD. Within the fields of cognitive psychology and cognitive neuroscience, there have been attempts to further understand the functions and the neural substrate of pSTM. However, fundamental questions concerning the role of pSTM in speech processing remain unanswered and little attempt have been made to translate these basic cognitive science studies to address vital clinical questions, specifically the centrality of deficits in pSTM as opposed to phonological representation and processes in DD. Consequently, the aim of the proposed research is twofold: First, we need to more clearly understand the relationship between phonological processing and pSTM processes and the extent to which they rely upon common or distinct neural substrates before we can establish where the deficit lies in DD. Hence the core components of this proposal focus on this initial step, where we aim to investigate the intersection of pSTM and phonological processing by assessing their overlapping neural networks. Secondly, we aim to extend this and make a step towards translating the results into clinical research addressing the question whether dyslexics’ deficit is more related to one or other, or common substrate impacts upon both."
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