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Developmental Expression of Amyloid Precursor Protein in Normal and Trisomy 16 Mice

  • Shannon Fisher
  • Mary Lou Oster-Granite
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 265)

Abstract

Down Syndrome (DS) or Trisomy 21 (Ts21) is the most common genetic cause of mental retardation in human newborns 1. While some DS individuals manifest cognitive decline as they age, those DS individuals who survive to become adults invariably have the neuropathologic stigmata of Alzheimer’s disease (AD) at autopsy 2. Overexpression of individual genes on human chromosome 21 (HSA 21) may contribute to the pathogenesis of these neuropathologic changes in both DS individuals and in AD patients 3. To explore this possibility, we study a model system, the trisomy 16 (Ts16) mouse. Mouse chromosome 16 (MMU 16) and HSA 21 exhibit significant genetic homology for a cluster of genes whose overexpression as a result of triplication is thought to contribute to the phenotypic characteristics of DS 4.

Keywords

Down Syndrome Alternate Splice Form Down Syndrome Brain Cerebrovascular Amyloid Normal Mouse Brain 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • Shannon Fisher
    • 1
  • Mary Lou Oster-Granite
    • 1
  1. 1.Developmental Genetics Laboratory of the Department of PhysiologyJohns Hopkins University School of MedicineBaltimoreUSA

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