Iron dysregulation in Huntington's disease

被引:95
作者
Muller, Michelle [1 ,2 ]
Leavitt, Blair R. [1 ,2 ,3 ,4 ]
机构
[1] Univ British Columbia, Dept Med Genet, Ctr Mol Med & Therapeut, Vancouver, BC V5Z 4H4, Canada
[2] Womens & Childrens Hosp, Vancouver, BC V5Z 4H4, Canada
[3] Univ British Columbia Hosp, Dept Med, Div Neurol, Vancouver, BC V6T 1W5, Canada
[4] Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 4H4, Canada
关键词
huntingtin; Huntington's disease; iron; magnetic resonance imaging; microglia; neurodegeneration; WILD-TYPE HUNTINGTIN; AGE-OF-ONSET; BRAIN TRANSITION-METALS; NMDA RECEPTOR FUNCTION; D-ASPARTATE RECEPTORS; N-TERMINAL FRAGMENTS; COMPLEX-II DEFECTS; RAS HOMOLOG RHES; MUTANT-HUNTINGTIN; OXIDATIVE STRESS;
D O I
10.1111/jnc.12739
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Huntington's disease (HD) is one of many neurodegenerative diseases with reported alterations in brain iron homeostasis that may contribute to neuropathogenesis. Iron accumulation in the specific brain areas of neurodegeneration in HD has been proposed based on observations in post-mortem tissue and magnetic resonance imaging studies. Altered magnetic resonance imaging signal within specific brain regions undergoing neurodegeneration has been consistently reported and interpreted as altered levels of brain iron. Biochemical studies using various techniques to measure iron species in human samples, mouse tissue, or in vitro has generated equivocal data to support such an association. Whether elevated brain iron occurs in HD, plays a significant contributing role in HD pathogenesis, or is a secondary effect remains currently unclear.
引用
收藏
页码:328 / 350
页数:23
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