Issue |
E3S Web Conf.
Volume 271, 2021
2021 2nd International Academic Conference on Energy Conservation, Environmental Protection and Energy Science (ICEPE 2021)
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Article Number | 03037 | |
Number of page(s) | 5 | |
Section | Research on Energy Chemistry and Chemical Simulation Performance | |
DOI | https://doi.org/10.1051/e3sconf/202127103037 | |
Published online | 15 June 2021 |
Factors of Cell Degeneration or Death caused by Mutant Tau Protein
Dalian Maple Leaf International High School, Liaoning 116650, China
* Corresponding author: 2017011423@students.maoleleafedu.com
Tau protein is a microtubule associated protein mainly expressed in neurons. Under pathological conditions, Tau protein is abnormally hyperphosphorylated and separated from microtubules. Abnormal Tau aggregates form nerve fiber tangles, which are insoluble aggregates in the brain. It is due to the microtubule rupture caused by Tau protein dysfunction and it is associated with neurofibrillar degeneration in Alzheimer's disease.This paper studies several reports and research on the structure and function of Tau protein, the role of Tau protein in pathological diseases and its relationship with neurodegenerative diseases. This paper concludes that Tau protein has undergone abnormal modification and aggregation in many neurodegenerative diseases, but the specific type of Tau protein that causes neurotoxicity, as well as the pathogenesis of its phosphorylation and functional injury inducing nerve apoptosis, are still not fully understood. Various abnormal modifications of Tau protein occur under pathological conditions, and fatal cascade events occur at different stages of neuron apoptosis. Therefore, the causes and effects of cytotoxicity mediated by Tau protein are very complicated. Different or even opposite conclusions are sometimes drawn in Tau protein-mediated neurodegeneration studies. This may be due to differences in Tau protein type, gene mutation and protein expression level.
© The Authors, published by EDP Sciences, 2021
This is an Open Access article distributed under the terms of the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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