Striatal mutant huntingtin protein levels decline with age in homozygous huntington's disease knock-in mouse models Academic Article uri icon

Overview

MeSH Major

  • Apoptosis
  • Arginase
  • Growth Substances
  • Motor Neurons
  • Nitric Oxide

abstract

  • A general decline in mutant HTT levels in striatum and cortex is observed that may contribute to disease progression in homozygous knock-in HD mouse models through reduction of HTT function. In cerebellum, sustained levels of mutant HTT with aging may be protective to this tissue which is less overtly affected in HD.

publication date

  • January 2018

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC6002862

Digital Object Identifier (DOI)

  • 10.3233/JHD-170274

PubMed ID

  • 29843246

Additional Document Info

start page

  • 137

end page

  • 150

volume

  • 7

number

  • 2