Document Detail


Neurocognitive development of attention across genetic syndromes Inspecting a disorder's dynamics through the lens of another.
MedLine Citation:
PMID:  21489395     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Information on the neural circuits underpinning adult attention has been heavily informed by the impact of distinct brain lesions on attentional processes. In a similar fashion, the genetics, molecular, and systems neuroscience of attention can be informed by the impact of developmental disorders of known genetic origin on attentional processes. Here, we focus on three developmental disorders of known genetic origin (Williams syndrome, Down syndrome, and fragile X syndrome) to appraise key findings to date, new developments, and their implications for the neurocognitive development of attention. This growing body of knowledge suggests that attention should be understood as a multicomponential construct whose component processes follow distinct but dynamically interacting developmental trajectories. Further, attentional processes act as critical gateways to further processing, memory, and learning, and they are by converse influenced by other developing skills. In turn, these interactions at the cognitive level emphasize the need to study developing neural circuits involved in attentional control in terms of how their coordinated operations may be modified over time by neural disorders, rather than construing them as isolated cortical or subcortical "modules for attention."
Authors:
Gaia Scerif; Ann Steele
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Progress in brain research     Volume:  189     ISSN:  1875-7855     ISO Abbreviation:  Prog. Brain Res.     Publication Date:  2011  
Date Detail:
Created Date:  2011-04-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376441     Medline TA:  Prog Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  285-301     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier B.V. All rights reserved.
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