Huntington’s disease mouse models: unraveling the pathology caused by CAG repeat expansion
Julia Kaye, Terry Reisine, Steven Finkbeiner
Abstract
locus, so a chimera of the full-length mouse protein with the N-terminal human portion is expressed. Many of aspects of the pathology and behavioral deficits in the KI model better mimic disease characteristics found in HD patients than other models. Accordingly, some have proposed that these mice may be preferable models of the disease over others. Indeed, as our understanding of HD advances, so will the design of animal models to test and develop HD therapies.
Topics & Concepts
Huntington's diseaseDiseaseTrinucleotide repeat expansionPathologyNeuroscienceBiologyMedicineGeneticsGeneAlleleGenetic Neurodegenerative DiseasesMitochondrial Function and PathologyNeurological disorders and treatments