Huntingtin (Htt) is a multi-function protein of the brain. Normal Htt shows a common alpha-helical structure but conformational changes in the form with beta strands are the principal cause of Huntington’s disease. Huntington’s disease is a genetic neurological disorder caused by a repeated expansion of the CAG trinucleotide, causing instability in the N-terminal of the gene coding for the Huntingtin protein. The mutation leads to the abnormal expansion of the production of the polyglutamine tract (polyQ) resulting in the form of an unstable Huntingtin protein commonly referred to as mutant Huntingtin. Mutant Huntingtin is the cause of the complex neurological metabolic alteration of Huntington’s disease, resulting in both the loss of all the functions of normal Huntingtin and the genesis of abnormal interactions due to the presence of this mutation. One of the problems arising from the misfolded Huntingtin is the increase in oxidative stress, which is common in many neurological diseases such as Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis and Creutzfeldt-Jakob disease. In the last few years, the use of antioxidants had a strong incentive to find valid therapies for defence against neurodegenerations. Although further studies are needed, the use of antioxidant mixtures to counteract neuronal damages seems promising.

亨廷顿（Htt）是大脑的一种多功能蛋白。正常Htt表现出常见的α螺旋结构，但β链形式的构象变化是亨廷顿氏病的主要原因。亨廷顿氏病是一种遗传神经系统疾病，由CAG三核苷酸的反复扩增引起，导致编码Huntingtin蛋白的基因N端不稳定。该突变导致聚谷氨酰胺束（polyQ）产生异常扩展，从而导致不稳定的亨廷顿蛋白形式，通常称为突变亨廷顿蛋白。亨廷顿蛋白突变是亨廷顿氏病复杂的神经代谢改变的原因，由于这种突变的存在，导致正常的亨廷顿蛋白的所有功能丧失和异常相互作用的产生。由亨廷顿蛋白错误折叠引起的问题之一是氧化应激的增加，这在许多神经系统疾病中很常见，例如阿尔茨海默氏病，帕金森氏病，肌萎缩性侧索硬化症和克雅氏病。在过去的几年中，抗氧化剂的使用强烈刺激了人们寻找有效的疗法来防御神经退行性变。尽管还需要进一步的研究，但使用抗氧化剂混合物来抵消神经元损伤似乎很有希望。肌萎缩性侧索硬化症和Creutzfeldt-Jakob病。在过去的几年中，抗氧化剂的使用强烈刺激了人们寻找有效的疗法来防御神经退行性变。尽管还需要进一步的研究，但使用抗氧化剂混合物来抵消神经元损伤似乎很有希望。肌萎缩性侧索硬化症和Creutzfeldt-Jakob病。在过去的几年中，抗氧化剂的使用强烈刺激了人们寻找有效的疗法来防御神经退行性变。尽管还需要进一步的研究，但使用抗氧化剂混合物来抵消神经元损伤似乎很有希望。