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March 1, 2000CellOpen Access

Reversal of Neuropathology and Motor Dysfunction in a Conditional Model of Huntington's Disease

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Authors

AYAi YamamotoTokyo University of AgricultureJLJosé J. LucasInstituto de Salud Carlos IIIRHRené HenUniversité de Tours

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Yamamoto et al. (2000) studied this question.

synapsesocial.com/papers/6aa26c7ca25963cecb13a01ehttps://doi.org/10.1016/s0092-8674(00)80623-6
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Decreased Neuronal and Increased Oligodendroglial Densities in Huntington's Disease Caudate Nucleus1991 · 245 citations
  2. 2Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells1999 · 450 citations
  3. 3Enhanced sensitivity to N-methyl-D-aspartate receptor activation in transgenic and knockin mouse models of Huntington's disease1999 · 354 citations
  4. 4Transgenic mice expressing a Huntington’s disease mutation are resistant to quinolinic acid-induced striatal excitotoxicity1999 · 229 citations
  5. 5Altered brain neurotransmitter receptors in transgenic mice expressing a portion of an abnormal human Huntington disease gene1998 · 504 citations