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A MOUSE MODEL FOR DOWN-SYNDROME EXHIBITS LEARNING AND BEHAVIOR DEFICITS
Author(s): REEVES RH, IRVING NG, MORAN TH, WOHN A, KITT C, SISODIA SS, SCHMIDT C, BRONSON RT, DAVISSON MT
Source: NATURE GENETICS    Volume: 11    Issue: 2    Pages: 177-184    Published: OCT 1995  
Times Cited: 308     References: 57     
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.
Document Type: Article
Language: English
Reprint Address: REEVES, RH (reprint author), JOHNS HOPKINS UNIV, SCH MED, DEPT PHYSIOL, 725 N WOLFE ST, BALTIMORE, MD 21205 USA
Addresses:
1. JOHNS HOPKINS UNIV, SCH MED, DEPT PSYCHIAT, BALTIMORE, MD 21205 USA
2. JOHNS HOPKINS UNIV, SCH MED, DEPT PATHOL, BALTIMORE, MD 21205 USA
3. JACKSON LAB, BAR HARBOR, ME 04609 USA
Publisher: NATURE PUBLISHING CO, 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707
Subject Category: Genetics & Heredity
IDS Number: RX806
ISSN: 1061-4036
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