2015
DOI: 10.1155/2015/151979
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Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?

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 tau… Show more

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Cited by 218 publications
(187 citation statements)
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References 209 publications
(226 reference statements)
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“…In the diseased brain, however, we postulate that conditions leading to aberrant tau hyperphosphorylation could favor the kinetics of droplet formation and stabilization—such as AD and FTD (Gong et al , 2005), elevated oxidative stress (Alavi Naini & Soussi‐Yanicostas, 2015), or traumatic brain injury (Blennow et al , 2012)—may favor the droplet state of tau, lead to increased droplet stability and droplet maturation, and eventually initiate tau aggregation. To what extent specific phosphorylation sites join this interplay of LLPS and aggregation remains to be explored.…”
Section: Discussionmentioning
confidence: 99%
“…In the diseased brain, however, we postulate that conditions leading to aberrant tau hyperphosphorylation could favor the kinetics of droplet formation and stabilization—such as AD and FTD (Gong et al , 2005), elevated oxidative stress (Alavi Naini & Soussi‐Yanicostas, 2015), or traumatic brain injury (Blennow et al , 2012)—may favor the droplet state of tau, lead to increased droplet stability and droplet maturation, and eventually initiate tau aggregation. To what extent specific phosphorylation sites join this interplay of LLPS and aggregation remains to be explored.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, the triple effects of LX2343 on neuroprotection, Aβ inhibition, and tau modulation indicate the potential of this multi-target compound in the treatment of AD. OS is a pivotal cellular response to the damage caused by tau toxicity, and the vicious interaction between these two causative events promotes AD progression [38] . Studies have identified OS as an early marker of tauopathy since OS and mitochondrial dysfunction are detected prior to tau hyperphosphorylation and NFT accumulation in tau P301S transgenic mice, which show tau hyperphosphorylation and tangle formation in 3 months [39] .…”
Section: Discussionmentioning
confidence: 99%
“…Studies have identified OS as an early marker of tauopathy since OS and mitochondrial dysfunction are detected prior to tau hyperphosphorylation and NFT accumulation in tau P301S transgenic mice, which show tau hyperphosphorylation and tangle formation in 3 months [39] . On the one hand, OS amplifies tauinduced neurotoxicity by induction of apoptosis and dysregulation of cell energy metabolism and promotes tau hyperphosphorylation and aggregation [38] . On the other hand, tauopathy induces OS [40] .…”
Section: Discussionmentioning
confidence: 99%
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“…For their part, actin ilaments are less susceptible to the negative efects of oxidative stress because they use ROS for their reorganization [44]. Finally, neuroilaments are phosphorylated in the presence of reactive species, which causes the formation of protein aggregates as the ones found in neurodegenerative diseases like Alzheimer's [45].…”
Section: Regulation Of the Dynamic Of The Cytoskeleton And The Efmentioning
confidence: 99%