Faculty Research 1990 - 1999

Title

A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments]

Document Type

Article

Publication Date

1995

Keywords

Amyloid-beta-Protein: bi, ge, Analysis-of-Variance, Animal, Chromosome-Mapping, Chromosomes-Human-Pair-21, Comparative-Study, Disease-Models-Animal, Down-Syndrome: ge, pp, px, pa, Female, Gene-Expression, Human, Learning, Male, Mice, Mice-Inbred-C3H, Mice-Inbred-C57BL, Mice-Neurologic-Mutants, Motor-Activity, Sex-Characteristics, SUPPORT-U-S-GOVT-P-H-S

JAX Source

Nat Genet 1995 Oct;11(2):177-84

Grant

HD24605/HD/NICHD, HD13131/HD/NICHD, HG00405/HG/NCHGR

Abstract

Trisomy 21 or Down syndrome (DS) is the most frequent genetic cause of mental retardation, affecting one in 800 live born human beings. Mice with segmental trisomy 16 (Ts65Dn mice) are at dosage imbalance for genes corresponding to those on human chromosome 21q21-22.3--which includes the so-called DS 'critical region'. They do not show early-onset of Alzheimer disease pathology; however, Ts65Dn mice do demonstrate impaired performance in a complex learning task requiring the integration of visual and spatial information. The reproducibility of this phenotype among Ts65Dn mice indicates that dosage imbalance for a gene or genes in this region contributes to this impairment. The corresponding dosage imbalance for the human homologues of these genes may contribute to cognitive deficits in DS.

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