Over-expression of RCAN1 causes Down syndrome-like hippocampal deficits that alter learning and memory
Katherine R Martin, Alicia Corlett, Daphne Dubach, Tomris Mustafa, Harold A Coleman, Helena C Parkington, Tobias D Merson, James A Bourne, Silvia Porta, Maria L Arbones, David I Finkelstein, Melanie A Pritchard
HUMAN MOLECULAR GENETICS | OXFORD UNIV PRESS | Published : 2012
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..View full abstract
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.