PUBLICATION
Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?
- Authors
- Alavi Naini, S.M., Soussi-Yanicostas, N.
- ID
- ZDB-PUB-150812-5
- Date
- 2015
- Source
- Oxidative Medinice and Cellular Longevity 2015: 151979 (Review)
- Registered Authors
- Soussi-Yanicostas, Nadia
- Keywords
- none
- MeSH Terms
-
- Brain/metabolism
- Humans
- Oxidative Stress*
- Phosphorylation
- Polymerization
- Protein Isoforms/genetics
- Protein Isoforms/metabolism
- Tauopathies/metabolism
- Tauopathies/pathology*
- tau Proteins/genetics
- tau Proteins/metabolism*
- PubMed
- 26576216 Full text @ Oxidative Med. and Cell. Long.
Citation
Alavi Naini, S.M., Soussi-Yanicostas, N. (2015) Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?. Oxidative Medinice and Cellular Longevity. 2015:151979.
Abstract
Hyperphosphorylation and aggregation of the microtubule-associated protein tau in brain, are pathological hallmarks of a
large family of neurodegenerative disorders, named tauopathies, which include Alzheimer’s disease. It has been shown that
increased phosphorylation of tau destabilizes tau-microtubule interactions, leading to microtubule instability, transport defects
along microtubules, and ultimately neuronal death. However, although mutations of the MAPT gene have been detected in
familial early-onset tauopathies, causative events in the more frequent sporadic late-onset forms and relationships between
tau hyperphosphorylation and neurodegeneration remain largely elusive. Oxidative stress is a further pathological hallmark of
tauopathies, but its precise role in the disease process is poorly understood. Another open question is the source of reactive oxygen
species, which induce oxidative stress in brain neurons. Mitochondria have been classically viewed as a major source for oxidative
stress, but microglial cells were recently identified as reactive oxygen species producers in tauopathies. Here we review the complex
relationships between tau pathology and oxidative stress, placing emphasis on (i) tau protein function, (ii) origin and consequences
of reactive oxygen species production, and (iii) links between tau phosphorylation and oxidative stress. Further, we go on to
discuss the hypothesis that tau hyperphosphorylation and oxidative stress are two key components of a vicious circle, crucial in
neurodegenerative tauopathies.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping