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Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease

View Article: PubMed Central - PubMed

ABSTRACT

Alzheimer's disease (AD) is the most common form of dementia characterized by progressive loss of memory and other cognitive functions among older people. Senile plaques and neurofibrillary tangles are the most hallmarks lesions in the brain of AD in addition to neurons loss. Accumulating evidence has shown that oxidative stress–induced damage may play an important role in the initiation and progression of AD pathogenesis. Redox impairment occurs when there is an imbalance between the production and quenching of free radicals from oxygen species. These reactive oxygen species augment the formation and aggregation of amyloid-β and tau protein hyperphosphorylation and vice versa. Currently, there is no available treatments can modify the disease. However, wide varieties of antioxidants show promise to delay or prevent the symptoms of AD and may help in treating the disease. In this review, the role of oxidative stress in AD pathogenesis and the common used antioxidant therapies for AD will summarize.

No MeSH data available.


Interventions between oxidative stress and the other key factors in AD.
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Figure 2: Interventions between oxidative stress and the other key factors in AD.

Mentions: Oxidative stress (OS) reflects the imbalance between the production and quenching of free radicals from oxygen species in the biological system. The disturbances in the normal redox status of cell can cause an increment in reactive oxygen species (ROS). These ROS play a key role in many chronic diseases including cancer, mitochondrial diseases [16], neurodegenerative diseases [17, 18]. Accumulating evidence has shown that the presence of extensive OS is a characteristic of AD brains in addition to the established pathology of senile plaques and NFT [19]. The interventions between OS and other key events in AD, which amplify the complexity of this issue was summarized in Fig. (2).


Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease
Interventions between oxidative stress and the other key factors in AD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384363&req=5

Figure 2: Interventions between oxidative stress and the other key factors in AD.
Mentions: Oxidative stress (OS) reflects the imbalance between the production and quenching of free radicals from oxygen species in the biological system. The disturbances in the normal redox status of cell can cause an increment in reactive oxygen species (ROS). These ROS play a key role in many chronic diseases including cancer, mitochondrial diseases [16], neurodegenerative diseases [17, 18]. Accumulating evidence has shown that the presence of extensive OS is a characteristic of AD brains in addition to the established pathology of senile plaques and NFT [19]. The interventions between OS and other key events in AD, which amplify the complexity of this issue was summarized in Fig. (2).

View Article: PubMed Central - PubMed

ABSTRACT

Alzheimer's disease (AD) is the most common form of dementia characterized by progressive loss of memory and other cognitive functions among older people. Senile plaques and neurofibrillary tangles are the most hallmarks lesions in the brain of AD in addition to neurons loss. Accumulating evidence has shown that oxidative stress–induced damage may play an important role in the initiation and progression of AD pathogenesis. Redox impairment occurs when there is an imbalance between the production and quenching of free radicals from oxygen species. These reactive oxygen species augment the formation and aggregation of amyloid-β and tau protein hyperphosphorylation and vice versa. Currently, there is no available treatments can modify the disease. However, wide varieties of antioxidants show promise to delay or prevent the symptoms of AD and may help in treating the disease. In this review, the role of oxidative stress in AD pathogenesis and the common used antioxidant therapies for AD will summarize.

No MeSH data available.