Mouse models of cognitive disorders in trisomy 21:: A review

被引：48

作者：

Seregaza, Zohra

Roubertoux, Pierre L.

Jamon, Marc

Soumireu-Mourat, Bernard

机构：

[1] Univ Mediterranee, UMR 6196, P3M, CNRS, F-13402 Marseille 20, France

[2] Univ Aix Marseille 1, Ctr St Charles, CNRS, UMR 6149, Marseille, France

来源：

BEHAVIOR GENETICS | 2006年 / 36卷 / 03期

关键词：

cognition; Down's syndrome; learning disorders; memory; mental retardation; transgenic mice; trisomy; 21;

D O I：

10.1007/s10519-006-9056-9

中图分类号：

B84 [心理学]; C [社会科学总论]; Q98 [人类学];

学科分类号：

03 ; 0303 ; 030303 ; 04 ; 0402 ;

摘要：

Trisomy 21 (TRS21) is the most frequent genetic cause of mental retardation. Although the presence of an extra copy of HSA21 is known to be at the origin of the syndrome, we do not know which 225 HSA21 genes have an effect on cognitive processes. Mouse models of TRS21 have been developed using syntenies between HSA21 and MMU16, MMU10 and MMU17. Available mouse models carry extra fragments of MMU16 or of HSA21 that cover all of HSA21 (chimeric HSA21) or MMU16 (Ts16); some carry large parts of MMU16 (Ts65Dn, Ts1Cje, Ms1Cje), while others have reduced contiguous fragments covering the D21S17-ETS2 region or single transfected genes. This offers a nest design strategy for deciphering cognitive (learning, memory and exploration) and associated brain abnormalities involving each of these chromosomal regions. This review confirms the crucial but not exclusive contribution of the D21S17-ETS2 region encompassing 16 genes to cognitive disorders.

引用

页码：387 / 404

页数：18

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