Mouse models for down syndrome-associated developmental cognitive disabilities

Chunhong Liu; Pavel V. Belichenko; Li Zhang; Dawei Fu; Alexander M. Kleschevnikov; Antonio Baldini; Stylianos E. Antonarakis; William C. Mobley; Y. Eugene Yu

doi:10.1159/000329422

Mouse models for down syndrome-associated developmental cognitive disabilities

Chunhong Liu, Pavel V. Belichenko, Li Zhang, Dawei Fu, Alexander M. Kleschevnikov, Antonio Baldini, Stylianos E. Antonarakis, William C. Mobley, Y. Eugene Yu

Research output: Contribution to journal › Review article › peer-review

40 Scopus citations

Abstract

Down syndrome (DS) is mainly caused by the presence of an extra copy of human chromosome 21 (Hsa21) and is a leading genetic cause for developmental cognitive disabilities in humans. The mouse is a premier model organism for DS because the regions on Hsa21 are syntenically conserved with three regions in the mouse genome, which are located on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. With the advance of chromosomal manipulation technologies, new mouse mutants have been generated to mimic DS at both the genotypic and phenotypic levels. Further mouse-based molecular genetic studies in the future may lead to the unraveling of the mechanisms underlying DS-associated developmental cognitive disabilities, which would lay the groundwork for developing effective treatments for this phenotypic manifestation. In this review, we will discuss recent progress and future challenges in modeling DS-associated developmental cognitive disability in mice with an emphasis on hippocampus-related phenotypes.

Original language	English (US)
Pages (from-to)	404-413
Number of pages	10
Journal	Developmental Neuroscience
Volume	33
Issue number	5
DOIs	https://doi.org/10.1159/000329422
State	Published - Nov 2011
Externally published	Yes

Keywords

Developmental cognitive disabilities
Down syndrome
Human trisomy 21
Mouse models
Targeted chromosome manipulation

ASJC Scopus subject areas

Neurology
Developmental Neuroscience

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10.1159/000329422

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title = "Mouse models for down syndrome-associated developmental cognitive disabilities",

abstract = "Down syndrome (DS) is mainly caused by the presence of an extra copy of human chromosome 21 (Hsa21) and is a leading genetic cause for developmental cognitive disabilities in humans. The mouse is a premier model organism for DS because the regions on Hsa21 are syntenically conserved with three regions in the mouse genome, which are located on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. With the advance of chromosomal manipulation technologies, new mouse mutants have been generated to mimic DS at both the genotypic and phenotypic levels. Further mouse-based molecular genetic studies in the future may lead to the unraveling of the mechanisms underlying DS-associated developmental cognitive disabilities, which would lay the groundwork for developing effective treatments for this phenotypic manifestation. In this review, we will discuss recent progress and future challenges in modeling DS-associated developmental cognitive disability in mice with an emphasis on hippocampus-related phenotypes.",

keywords = "Developmental cognitive disabilities, Down syndrome, Human trisomy 21, Mouse models, Targeted chromosome manipulation",

author = "Chunhong Liu and Belichenko, {Pavel V.} and Li Zhang and Dawei Fu and Kleschevnikov, {Alexander M.} and Antonio Baldini and Antonarakis, {Stylianos E.} and Mobley, {William C.} and Yu, {Y. Eugene}",

year = "2011",

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doi = "10.1159/000329422",

language = "English (US)",

volume = "33",

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AU - Liu, Chunhong

AU - Belichenko, Pavel V.

AU - Zhang, Li

AU - Fu, Dawei

AU - Kleschevnikov, Alexander M.

AU - Baldini, Antonio

AU - Antonarakis, Stylianos E.

AU - Mobley, William C.

AU - Yu, Y. Eugene

PY - 2011/11

Y1 - 2011/11

N2 - Down syndrome (DS) is mainly caused by the presence of an extra copy of human chromosome 21 (Hsa21) and is a leading genetic cause for developmental cognitive disabilities in humans. The mouse is a premier model organism for DS because the regions on Hsa21 are syntenically conserved with three regions in the mouse genome, which are located on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. With the advance of chromosomal manipulation technologies, new mouse mutants have been generated to mimic DS at both the genotypic and phenotypic levels. Further mouse-based molecular genetic studies in the future may lead to the unraveling of the mechanisms underlying DS-associated developmental cognitive disabilities, which would lay the groundwork for developing effective treatments for this phenotypic manifestation. In this review, we will discuss recent progress and future challenges in modeling DS-associated developmental cognitive disability in mice with an emphasis on hippocampus-related phenotypes.

AB - Down syndrome (DS) is mainly caused by the presence of an extra copy of human chromosome 21 (Hsa21) and is a leading genetic cause for developmental cognitive disabilities in humans. The mouse is a premier model organism for DS because the regions on Hsa21 are syntenically conserved with three regions in the mouse genome, which are located on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. With the advance of chromosomal manipulation technologies, new mouse mutants have been generated to mimic DS at both the genotypic and phenotypic levels. Further mouse-based molecular genetic studies in the future may lead to the unraveling of the mechanisms underlying DS-associated developmental cognitive disabilities, which would lay the groundwork for developing effective treatments for this phenotypic manifestation. In this review, we will discuss recent progress and future challenges in modeling DS-associated developmental cognitive disability in mice with an emphasis on hippocampus-related phenotypes.

KW - Developmental cognitive disabilities

KW - Down syndrome

KW - Human trisomy 21

KW - Mouse models

KW - Targeted chromosome manipulation

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JO - Developmental Neuroscience

JF - Developmental Neuroscience

IS - 5

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Mouse models for down syndrome-associated developmental cognitive disabilities

Abstract

Keywords

ASJC Scopus subject areas

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