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ERIC Number: EJ892919
Record Type: Journal
Publication Date: 2010-Mar
Pages: 30
Abstractor: As Provided
Reference Count: 0
ISSN: ISSN-1944-7515
Molecular and Cellular Mechanisms Elucidating Neurocognitive Basis of Functional Impairments Associated with Intellectual Disability in Down Syndrome
Rachidi, Mohammed; Lopes, Carmela
American Journal on Intellectual and Developmental Disabilities, v115 n2 p83-112 Mar 2010
Down syndrome, the most common genetic cause of intellectual disability, is associated with brain disorders due to chromosome 21 gene overdosage. Molecular and cellular mechanisms involved in the neuromorphological alterations and cognitive impairments are reported herein in a global model. Recent advances in Down syndrome research have lead to the identification of altered molecular pathways involved in intellectual disability, such as Calcineurin/NFATs pathways, that are of crucial importance in understanding the molecular basis of intellectual disability pathogenesis in this syndrome. Potential treatments in mouse models of Down syndrome, including antagonists of NMDA or GABA[subscript A] receptors, and microRNAs provide new avenues to develop treatments of intellectual disability. Nevertheless, understanding the links between molecular pathways and treatment strategies in human beings requires further research.
American Association on Intellectual and Developmental Disabilities. P.O. Box 1897, Lawrence, KS 66044-1897. Tel: 785-843-1235; Fax: 785-843-1274; e-mail:; Web site:
Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A