scholarly journals The Cascade of Oxidative Stress and Tau Protein Autophagic Dysfunction in Alzheimer’s Disease

10.5772/59980 ◽  
2015 ◽  
Author(s):  
Zhenzhen Liu ◽  
Peifu Li ◽  
Jiannan Wu ◽  
Yi Wang ◽  
Ping Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein

scholarly journals Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 146
Author(s):  
Ryszard Pluta ◽  
Jacek Kiś ◽  
Sławomir Januszewski ◽  
Mirosław Jabłoński ◽  
Stanisław J. Czuczwar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Damage ◽  
Free Radicals ◽  
Brain Ischemia ◽  
Tau Protein ◽  
Dna Damage And Repair ◽  
Ischemic Brain ◽  
Remarkable Progress

Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy.

P3-085: Interaction network of tau protein, beta-amyloid protein, and amyloid protein precursor under oxidative stress in Alzheimer's disease

2015 ◽  
Vol 11 (7S_Part_14) ◽  
pp. P651-P652
Author(s):  
Eduardo de SouzaS. Nicolau ◽  
Ana Paula Mendes Silva ◽  
Kenia Kelly Fiaux do Nascimento ◽  
Kelly Silva Pereira ◽  
Gizele Ribeiro dos Santos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Interaction Network ◽  
Beta Amyloid ◽  
Amyloid Protein ◽  
Protein Precursor ◽  
Amyloid Protein Precursor ◽  
Beta Amyloid Protein

scholarly journals Phosphorylation of Tau Protein as the Link between Oxidative Stress, Mitochondrial Dysfunction, and Connectivity Failure: Implications for Alzheimer’s Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Siddhartha Mondragón-Rodríguez ◽  
George Perry ◽  
Xiongwei Zhu ◽  
Paula I. Moreira ◽  
Mariana C. Acevedo-Aquino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Complex Disease ◽  
Therapeutic Option ◽  
Combined Therapy ◽  
Phosphorylated Tau ◽  
Neurite Degeneration ◽  
Phosphorylated Tau Protein

Alzheimer’s disease (AD) is defined by the concurrence of abnormal aggregates composed of phosphorylated tau protein and of abnormal cellular changes including neurite degeneration, loss of neurons, and loss of cognitive functions. While a number of mechanisms have been implicated in this complex disease, oxidative stress remains one of the earliest and strongest events related to disease progression. However, the mechanism that links oxidative stress and cognitive decline remains elusive. Here, we propose that phosphorylated tau protein could be playing the role of potential connector and, therefore, that a combined therapy involving antioxidants and check points for synaptic plasticity during early stages of the disease could become a viable therapeutic option for AD treatment.

scholarly journals Role of Oxygen Radicals in Alzheimer’s Disease: Focus on Tau Protein

Oxygen ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 96-120
Author(s):  
Anna Atlante ◽  
Daniela Valenti ◽  
Valentina Latina ◽  
Giuseppina Amadoro
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Posttranslational Modifications ◽  
Oxygen Radicals ◽  
Oxygen Free Radical ◽  
Transgenic Animal ◽  
Early Event

Oxygen free radical burst is a prominent early event in the pathogenesis of Alzheimer’s disease (AD). Posttranslational modifications of Tau protein, primarily hyper-phosphorylation and truncation, are indicated as critical mediators of AD pathology. This finding is confirmed by the high levels of oxidative stress markers and by the increased susceptibility to oxygen radicals found in cultured neurons and in brains from transgenic animal models expressing toxic Tau forms, in concomitance with a dramatic reduction in their viability/survival. Here, we collect the latest progress in research focused on the reciprocal and dynamic interplay between oxygen radicals and pathological Tau, discussing how these harmful species cooperate and/or synergize in the progression of AD. In this context, a better understanding of the role of oxidative stress in determining Tau pathology, and vice versa, primarily could be able to define novel biomarkers of early stages of human tauopathies, including AD, and then to develop therapeutic strategies aimed at attenuating, halting, or reversing disease progression.

Oxidative Stress and Amyloid Beta Toxicity in Alzheimer’s Disease: Intervention in a Complex Relationship by Antioxidants

2013 ◽  
Vol 20 (37) ◽  
pp. 4648-4664 ◽  
Author(s):  
S. Chakrabarti ◽  
M. Sinha ◽  
I. Thakurta ◽  
P. Banerjee ◽  
M. Chattopadhyay
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Complex Relationship
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