The tubulin-associated unit (Tau) protein is an intrinsically disordered protein that plays a well-established role in promoting microtubule assembly and regulation of microtubule dynamics in neuronal axons at all stages of development. Identification of new interacting partners and different sub-cellular localizations of Tau in recent years led to the discovery of novel physiological functions in regulation of neuronal activity, neurogenesis, long-term depression, iron export and genomic integrity. In addition, Tau gene mutations, aberrant mRNA splicing and abnormal post-translational modifications, such as hyperphosphorylation, lead to formation of pathological, insoluble Tau aggregates that are a hallmark of neurodegenerative diseases, collectively known as tauopathies. Characterized by synaptic dysfunction, neuroinflammation/neuronal cell death and dementia, tauopathies are designated as a group of adult-onset neurodegenerative diseases. Recent studies summarized in this review document several neurological conditions and diseases in an early life stage with upregulated levels or even pathological aggregation of abnormally phosphorylated Tau protein. These findings suggest that Tau might play a previously underestimated role in neurodevelopmental disorders and regression in children.

微管蛋白相关单位（Tau）蛋白是一种内在失调的蛋白，在发育的各个阶段都在促进神经元轴突中的微管组装和微管动力学调节方面起着公认的作用。近年来，新的相互作用伴侣和Tau的不同亚细胞定位的鉴定导致了在调节神经元活性，神经发生，长期抑郁，铁输出和基因组完整性方面新的生理功能的发现。此外，Tau基因突变，异常的mRNA剪接和异常的翻译后修饰（如磷酸化过高）会导致形成病理性的，不可溶的Tau聚集体，这些聚集体是神经退行性疾病的标志，统称为tauopathies。以突触功能障碍为特征 神经炎症/神经细胞死亡和痴呆，tauopathies被指定为一组成人发病的神经退行性疾病。这篇综述中总结的最新研究记录了生命早期阶段的几种神经系统疾病和疾病，其异常磷酸化的Tau蛋白水平升高甚至发生病理性聚集。这些发现表明，Tau可能在儿童神经发育障碍和消退中起着被低估的作用。