Over the past twenty years there have been numerous advances in our understanding of Huntington's disease (HD) and other neurodegenerative proteopathies such as Alzheimer's disease and Parkinson's disease. In each case, disease-specific proteins are expressed and accumulate; what has been less clear is precisely what problems are caused by the accumulation. Recently we have begun to appreciate that increased protein levels or changes in the ratios of different isoforms affect the movement of molecules along the axon, thereby disrupting neuronal function. Huntingtin, the protein involved in HD, plays a special role in axonal transport, and very recent studies have found that its activity - and the movement of its cargoes - is altered not only in HD but in other neurological diseases. Here, we contextualize these studies and consider how modulating huntingtin activity could provide new avenues to therapy.

中文翻译：

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交通信号：神经疾病中亨廷顿蛋白和轴突运输的新功能。

在过去的二十年中，我们对亨廷顿氏病（HD）和其他神经退行性蛋白病（例如阿尔茨海默氏病和帕金森氏病）的理解取得了许多进步。在每种情况下，特定疾病的蛋白质都会表达并积累。尚不清楚的是正是由累积引起的问题。最近，我们开始意识到增加的蛋白质水平或不同同种型比率的变化会影响分子沿轴突的运动，从而破坏神经元功能。亨廷顿蛋白是一种参与HD的蛋白，在轴突运输中起着特殊作用，最近的研究发现，其活性以及其货物的移动不仅在HD中而且在其他神经系统疾病中都发生了改变。这里，