Cognitive and pharmacological insights from the Ts65Dn mouse model of Down syndrome

被引:18
作者
Ruparelia, Aarti [2 ]
Pearn, Matthew L. [3 ,4 ]
Mobley, William C. [1 ]
机构
[1] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA
[2] UCL Inst Neurol, Dept Neurodegenerat Dis, London WC1N 3BG, England
[3] Univ Calif San Diego, Dept Anaesthesiol, La Jolla, CA 92093 USA
[4] VA San Diego Healthcare Syst, San Diego, CA 92161 USA
关键词
LONG-TERM POTENTIATION; RESTORES NEUROGENESIS; DEFICITS; DYRK1A; ABNORMALITIES; MEMANTINE; CELLS; MICE; NEUROTRANSMISSION; PHARMACOTHERAPY;
D O I
10.1016/j.conb.2012.05.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Down syndrome (DS) is a multi-faceted condition resulting in the most common genetic form of intellectual disability. Mouse models of DS, especially the Ts65Dn model, have been pivotal in furthering our understanding of the genetic, molecular and neurobiological mechanisms that underlie learning and memory impairments in DS. Cognitive and pharmacological insights from the Ts65Dn mouse model have led to remarkable translational progress in the development of therapeutic targets and in the emergence of DS clinical trials. Unravelling the pathogenic role of trisomic genes on human chromosome 21 and the genotype-phenotype relationship still remains a pertinent goal for tackling cognitive deficits in DS.
引用
收藏
页码:880 / 886
页数:7
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