Faculty Research 1990 - 1999
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
First Page
177
Last Page
184
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.
Recommended Citation
Reeves RH,
Irving NG,
Moran TH,
Wohn A,
Kitt C,
Sisodia SS,
Schmidt C,
Bronson RT,
Davisson MT.
A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments] Nat Genet 1995 Oct;11(2):177-84