Department of Medical Genetics, Centre for Molecular Medicine & Therapeutics, University of British Columbia and Children's and Women's Hospital, Vancouver, British Columbia, Canada.
J Neurochem. 2014 Aug;130(3):328-50. doi: 10.1111/jnc.12739. Epub 2014 May 28.
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.
亨廷顿病(HD)是许多神经退行性疾病之一,据报道其脑铁动态平衡发生改变,可能导致神经发病机制。基于对死后组织和磁共振成像研究的观察,提出了 HD 中神经退行性变特定脑区铁积累的假说。在经历神经退行性变的特定脑区,磁共振成像信号的改变已被一致报道,并被解释为脑铁水平的改变。使用各种技术在人体样本、小鼠组织或体外测量铁种类的生化研究产生了模棱两可的数据来支持这种关联。升高的脑铁是否发生在 HD 中,是否在 HD 发病机制中起重要作用,还是继发效应,目前尚不清楚。