Journal article
Over-expression of RCAN1 causes down syndrome-like hippocampal deficits that alter learning and memory
KR Martin, A Corlett, D Dubach, T Mustafa, HA Coleman, HC Parkington, TD Merson, JA Bourne, S Porta, ML Arbonés, DI Finkelstein, MA Pritchard
Human Molecular Genetics | Published : 2012
DOI: 10.1093/hmg/dds134
Abstract
People with Down syndrome (DS) exhibit abnormal brain structure. Alterations affecting neurotransmission and signalling pathways that govern brain function are also evident. A large number of genes are simultaneously expressed at abnormal levels in DS; therefore, it is a challenge to determine which gene(s) contribute to specific abnormalities, and then identify the key molecular pathways involved. We generated RCAN1-TG mice to study the consequences of RCAN1 over-expression and investigate the contribution of RCAN1 to the brain phenotype of DS. RCAN1-TG mice exhibit structural brain abnormalities in those areas affected in DS. The volume and number of neurons within the hippocampus is reduc..
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Funding Acknowledgements
This work was supported by the Fondation Jerome Lejeune; philanthropic grants from the Judith Jane Mason & Harold Stannett Williams Memorial Foundation managed by ANZ Trustees; the APEX Foundation for Research into Intellectual Disability; the CASS Foundation; and the L.E.W. Carty Charitable Fund.