Abstract
Tauopathy is a collective term for neurodegenerative diseases associated with pathological modifications of tau protein. Tau modifications are mediated by many factors. Recently, reactive oxygen species (ROS) have attracted attention due to their upstream and downstream effects on tauopathy. In physiological conditions, healthy cells generate a moderate level of ROS for self-defense against foreign invaders. Imbalances between ROS and the anti-oxidation pathway cause an accumulation of excessive ROS. There is clear evidence that ROS directly promotes tau modifications in tauopathy. ROS is also highly upregulated in the patients’ brain of tauopathies, and anti-oxidants are currently prescribed as potential therapeutic agents for tauopathy. Thus, there is a clear connection between oxidative stress (OS) and tauopathies that needs to be studied in more detail. In this review, we will describe the chemical nature of ROS and their roles in tauopathy.
Highlights
Molecular Recognition Research Center, Korea Institute of Science and Technology (KIST), Seoul 02792, Bio-Med Division, KIST-School UST, Seoul 02792, Korea
The level of neurofibrillary tangle (NFT) and tau modifications are correlated to the severity of the tauopathies, including Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD), FTD with parkinsonism linked to chromosome-17 (FTDP-17), frontotemporal lobar degeneration (FTLD), Pick’s disease (PiD), progressive supranuclear palsy (PSP), corticobasal neurodegeneration (CBD), dementia pugilistica, etc. [9,10,11,12]
A few of the main features about the role of reduction potential and reactivity are listed as follows: (a) Reduction potential is the ability of an atom or molecule to acquire the electron; (b) oxidation is the loss of electron, whereas reduction is the gain of electron; and (c) from the above points, it is evident that atoms or molecules with high reductionhave potential have highasreactivity as will be easy to reduce
Summary
Tau protein is expressed abundantly in neurons as well as sparsely in non-neuronal cells like astrocytes and oligodendrocytes [1]. It is a microtubule-binding protein that gives microtubules’. Tau modification is promoted by post-translational modifications, conformational changes and the misfolding structure of tau. These modifications lead to the abnormal aggregation of tau into neurofibrillary tangle (NFT). The level of NFTs and tau modifications are correlated to the severity of the tauopathies, including Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD), FTD with parkinsonism linked to chromosome-17 (FTDP-17), frontotemporal lobar degeneration (FTLD), Pick’s disease (PiD), progressive supranuclear palsy (PSP), corticobasal neurodegeneration (CBD), dementia pugilistica, etc. The level of NFTs and tau modifications are correlated to the severity of the tauopathies, including Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD), FTD with parkinsonism linked to chromosome-17 (FTDP-17), frontotemporal lobar degeneration (FTLD), Pick’s disease (PiD), progressive supranuclear palsy (PSP), corticobasal neurodegeneration (CBD), dementia pugilistica, etc. [9,10,11,12]
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