Extensive studies on PINK1, whose mutations are a confirmed cause of Parkinson’s disease (PD), have been conducted in animal models or immortalized cell lines. These include initial ground-breaking discoveries on mitophagy, which demonstrated that PINK1 recruits Parkin on depolarized mitochondria, initiating a signalling cascade eventually resulting in their autophagic degradation. Not all features of this complex molecular pathway have been reproduced in mammalian or human neurons, undermining the hypothesis proposing mitophagy as the most relevant biochemical link between PINK1 deficiency and PD pathogenesis.

Experiments in murine primary neurons examined another possible neuroprotective function of PINK1, namely its involvement in mitochondrial motility along axons and dendrites. PINK1 interacts with Miro, a component of the motor/adaptor complex binding mitochondria to microtubules and allowing their movement to and from cellular processes. Distinct subcellular pools of PINK1, cytosolic and mitochondrial, appear to regulate anterograde and retrograde transport, respectively.

Technological advancements today allow researchers to de-differentiate fibroblasts into induced pluripotent stem cells and re-differentiate them into dopaminergic neurons. Few studies based on this technique address possible neuroprotective effects of PINK1, including mitophagy and mitochondrial homeostasis, but underline the need for a broader characterization of its function in neurons.

已在动物模型或永生化细胞系中进行了对PINK1的广泛研究，其突变是帕金森氏病（PD）的确定原因。这些包括线粒体的开创性发现，这表明PINK1在去极化的线粒体上募集了Parkin，启动了信号传导级联反应，最终导致其自噬降解。并非这种复杂的分子途径的所有特征都已经在哺乳动物或人类的神经元中复制，从而破坏了认为线粒化是PINK1缺乏与PD发病机理之间最相关的生化联系的假说。

在鼠原代神经元中进行的实验检查了PINK1的另一种可能的神经保护功能，即其参与了沿轴突和树突的线粒体运动。PINK1与Miro相互作用，Miro是将线粒体结合到微管的运动/适配器复合物的一个组成部分，并允许其在细胞过程中移动。PINK1，胞质和线粒体的不同亚细胞库似乎分别调节顺行和逆行运输。

当今的技术进步使研究人员能够将成纤维细胞脱分化为诱导性多能干细胞，并将它们重新分化为多巴胺能神经元。基于这项技术的研究很少涉及PINK1的可能的神经保护作用，包括线粒体和线粒体的体内平衡，但强调需要对其神经元功能进行更广泛的表征。