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- SPONTANEOUS PARTIAL TRISOMY 16 MICE AS MODELS FOR HUMAN DOWN SYNDROME
- DOSAGE-DEPENDENT OVEREXPRESSION OF GENES ON TRISOMIC SEGMENT OF THE DS MOUSE MODEL
- EXCESSIVE OXIDATIVE STRESS, IMPAIRED NEUROGENESIS AND VENTRICULAR ENLARGEMENTS IN THE BRAINS OF DS MOUSE MODELS
- PREFERABLE STRATEGY TO IDENTIFY THE GENES FOR DS: RESUMPTIONS OF THE COPY NUMBER OF CANDIDATE GENES IN DS MOUSE MODELS
- HIGHLY EFFICIENT SYSTEM FOR THE GENERATION OF DS MOUSE MODELS WITH DESIGNED PARTIAL TRISOMY SEGMENTS THAT HARBORS MULTIPLE GENE KNOCKOUTS
Down syndrome (DS) is the most common cause of mental retardation. Several DS mouse models with partial trisomy 16 homologous to human chromosome 21 have been developed, and our research group has been studying those mouse models. We have shown a dosage-dependent overexpression of genes in the trisomic region of the mouse. We have also described abnormalities including increased oxidative stress, increased lipid peroxidation, mitochondrial dysfunction, tau-hyperphosphorylation and overactivation of its phosphatases, impaired developmental and adult neurogenesis, histological abnormalities in brains including ventricle enlargements and minor neurodegenerations in those mice. These observations may contribute to the identification of responsible genes and understanding of molecular pathology of Down syndrome.