School of Mechanical and Manufacturing Engineering (SMME), National University of Sciences and Technology (NUST), Bolan Road, Sector H-12, Islamabad, 46000, Pakistan.
Clinical Department of Neurology, University Medical Center Göttingen and the German Center for Neurodegenerative Diseases (DZNE), Robert-Koch-Straße 40, 37075, Göttingen, Germany.
Mol Neurobiol. 2023 Sep;60(9):5155-5166. doi: 10.1007/s12035-023-03387-8. Epub 2023 Jun 2.
Tau is a microtubule-associated binding protein in the nervous system that is known for its role in stabilizing microtubules throughout the nerve cell. It accumulates as β-sheet-rich aggregates and neurofibrillary tangles, leading to an array of different pathologies. Six splice variants of this protein, generated from the microtubule-associated protein tau (MAPT) gene, are expressed in the brain. Amongst these variants, 0N3R, is prominent during fetal development, while the rest, 0N4R, 1N3R, 1N4R, 2N3R, and 2N4R, are expressed in postnatal stages. Tau isoforms play their role separately or in combination with others to contribute to one or multiple neurodegenerative disorders and clinical syndromes. For instance, in Alzheimer's disease and a subset of frontotemporal lobar degeneration (FTLD)-MAPT (i.e., R406W and V337M), both 3R and 4R isoforms are involved; therefore, they are called 3R/4R mix tauopathies. On the other hand, 4R isoforms are aggregated in progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and a majority of FTLD-MAPT and these diseases are called 4R tauopathies. Similarly, Pick's disease has an association with 3R tau isoforms and is thereby referred to as 3R tauopathy. Unlike 3R isoforms, the 4R variants have a faster rate of aggregation that accelerates the associated neurodegenerative mechanisms. Moreover, post-translational modifications of each isoform occur at a different rate and dictate their physiological and pathological attributes. The smallest tau isoform (0N3R) is highly phosphorylated in the fetal brain but does not lead to the generation of aggregates. On the other hand, proteoforms in the adult human brain undergo aggregation upon their phosphorylation and glycation. Expanding on this knowledge, this article aims to review the physiological and pathological roles of tau isoforms and their underlying mechanisms that result in neurological deficits. Physiological and pathological relevance of microtubule-associated protein tau (MAPT): Tau exists as six splice variants in the brain, each differing with respect to expression, post-translational modifications (PTMs), and aggregation kinetics. Physiologically, they are involved in the stabilization of microtubules that form the molecular highways for axonal transport. However, an imbalance in their expression and the associated PTMs leads to a disruption in their physiological function through the formation of neurofibrillary tangles that accumulate in various regions of the brain and contribute to several types of tauopathies.
Tau 是神经系统中的一种微管相关结合蛋白,其功能是稳定神经细胞中的微管。Tau 会聚集形成富含β-片层的聚集物和神经纤维缠结,导致多种不同的病理变化。该蛋白有六种剪接变体,由微管相关蛋白 tau(MAPT)基因产生,在大脑中表达。其中,0N3R 在胎儿发育过程中较为突出,而其余变体,0N4R、1N3R、1N4R、2N3R 和 2N4R,在出生后阶段表达。Tau 异构体分别或与其他异构体组合发挥作用,导致一种或多种神经退行性疾病和临床综合征。例如,在阿尔茨海默病和额颞叶变性(FTLD)-MAPT 的一个亚组(即 R406W 和 V337M)中,3R 和 4R 异构体都参与其中,因此被称为 3R/4R 混合 tau 病。另一方面,4R 异构体在进行性核上性麻痹(PSP)、皮质基底节变性(CBD)和大多数 FTLD-MAPT 中聚集,这些疾病被称为 4R tau 病。同样,匹克病与 3R tau 异构体有关,因此被称为 3R tau 病。与 3R 异构体不同,4R 变体的聚集速度更快,加速了相关的神经退行性机制。此外,每种异构体的翻译后修饰发生的速度不同,并决定了它们的生理和病理属性。最小的 tau 异构体(0N3R)在胎儿脑中高度磷酸化,但不会导致聚集物的产生。另一方面,成人脑中的蛋白水解产物在磷酸化和糖基化后会发生聚集。基于这方面的知识,本文旨在综述 tau 异构体的生理和病理作用及其导致神经功能缺陷的潜在机制。微管相关蛋白 tau(MAPT)的生理和病理相关性:tau 在脑中以六种剪接变体的形式存在,每种变体在表达、翻译后修饰(PTMs)和聚集动力学方面都有所不同。在生理上,它们参与稳定形成轴突运输分子高速公路的微管。然而,其表达和相关 PTMs 的失衡会通过形成神经纤维缠结导致其生理功能紊乱,这些缠结在大脑的不同区域积累,并导致多种 tau 病。