The role of mitochondrial defects and oxidative stress in Alzheimer’s disease

2019 ◽  
Vol 27 (9) ◽  
pp. 932-942 ◽  
Author(s):  
Badar ul Islam ◽  
Nasimudeen R Jabir ◽  
Shams Tabrez
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mitochondrial Defects ◽  
And Oxidative Stress

Vascular cognitive impairment and Alzheimer’s disease: role of cerebral hypoperfusion and oxidative stress

2012 ◽  
Vol 385 (10) ◽  
pp. 953-959 ◽  
Author(s):  
Hyun Ah Kim ◽  
Alyson A. Miller ◽  
Grant R. Drummond ◽  
Amanda G. Thrift ◽  
Thiruma V. Arumugam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Vascular Cognitive Impairment ◽  
Cerebral Hypoperfusion ◽  
And Oxidative Stress

scholarly journals Role of antioxidants and a nutrient rich diet in Alzheimer's disease

Open Biology ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 200084 ◽  
Author(s):  
Gerald Veurink ◽  
George Perry ◽  
Sandeep Kumar Singh
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Metabolic Acidosis ◽  
Synergistic Effects ◽  
The Body ◽  
High Dose ◽  
Degenerative Diseases ◽  
And Oxidative Stress

The joint attack on the body by metabolic acidosis and oxidative stress suggests that treatment in degenerative diseases, including Alzheimer's disease (AD), may require a normalizing of extracellular and intracellular pH with simultaneous supplementation of an antioxidant combination cocktail at a sufficiently high dose. Evidence is also accumulating that combinations of antioxidants may be more effective, taking advantage of synergistic effects of appropriate antioxidants as well as a nutrient-rich diet to prevent and reverse AD. This review focuses on nutritional, nutraceutical and antioxidant treatments of AD, although they can also be used in other chronic degenerative and neurodegenerative diseases.

scholarly journals Role of Methylglyoxal in Alzheimer’s Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Cristina Angeloni ◽  
Laura Zambonin ◽  
Silvana Hrelia
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Advanced Glycation ◽  
Hyperphosphorylated Tau Protein ◽  
Glycation End Products ◽  
And Oxidative Stress ◽  
Endogenous Process

Alzheimer’s disease is the most common and lethal neurodegenerative disorder. The major hallmarks of Alzheimer’s disease are extracellular aggregation of amyloidβpeptides and, the presence of intracellular neurofibrillary tangles formed by precipitation/aggregation of hyperphosphorylated tau protein. The etiology of Alzheimer’s disease is multifactorial and a full understanding of its pathogenesis remains elusive. Some years ago, it has been suggested that glycation may contribute to both extensive protein cross-linking and oxidative stress in Alzheimer’s disease. Glycation is an endogenous process that leads to the production of a class of compounds known as advanced glycation end products (AGEs). Interestingly, increased levels of AGEs have been observed in brains of Alzheimer’s disease patients. Methylglyoxal, a reactive intermediate of cellular metabolism, is the most potent precursor of AGEs and is strictly correlated with an increase of oxidative stress in Alzheimer’s disease. Many studies are showing that methylglyoxal and methylglyoxal-derived AGEs play a key role in the etiopathogenesis of Alzheimer's disease.

scholarly journals The role of mitochondria-targeted antioxidant MitoQ in neurodegenerative disease

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Linlin Zhang ◽  
Aurelio Reyes ◽  
Xiangdong Wang
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disease ◽  
And Oxidative Stress

The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondria-targeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.

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