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Mouse Model Of Down Syndrome Offers Glimpse Into Role Of Specific Genes In TheDisorder

in humans. And this, said Huang, should make it easier to zero in on the role of individual genes.

Another previous standard model, Ts65Dn, includes a slightly larger third segment of chromosome 16 and causes more widespread learning and behavioral impairments than the newer model.

The researchers plan to tease out the specific role of genes in the newer model by using the older model as a backdrop.

"By analyzing this mouse model side-by-side with Ts65Dn," said Huang, "we can see what kind of physiological and biochemical differences there are between the two, and this may enable us to identify the role of some of the specific genes involved. Ultimately, we may be able to make corrections in these animals." The new mouse model includes approximately 20 genes that have been identified on the extra segment of chromosome 16 in the previous models.

The researchers say it is too early to draw strict parallels between the cognitive deficits in humans with Down syndrome and the learning, behavioral and structural abnormalities observed in the genetically engineered mice. However, they said, their new mouse model should yield insights into the chromosomal regions and the genes they contain that have the capability of disturbing neuronal structure and function when present in an extra copy. And the mechanisms by which these perturbations occur, they said, are likely to be relevant to the human situation.

In addition, they said, these animals can be used to assess potential pharmacological agents and various forms of environmental enrichment for their ability to improve learning and behavior. Already, the researchers have been able to improve the spatial learning deficits in the mice with training. In mice in the older, Ts65Dn model, the researchers succeeded in reversing neurodegeneration of one form of neuron with the use of nerve growth factor. "We have a ways to go," said Epstein, a professor of pediatrics and a senior author of the study, "but we're
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Contact: Jennifer O'Brien
jobrien@itsa.ucsf.edu
(415) 476-2557
University of California - San Francisco
1-Jun-1998


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