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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.


Chemical structure of α-tocopherol form of vitamin E (C29H50O2).
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Figure 8: Chemical structure of α-tocopherol form of vitamin E (C29H50O2).

Mentions: There are two groups of vitamin E with different ten forms; five as tocotrienols and five as tocopherols and identified by α-, β-, γ-, δ- and ε-. The most biologically active form of vitamin E is α-tocopherol (Fig. 8). The work of Sano et al. [118] gave impetus to the idea of vitamin E as the treatment of AD. At the present days, the same group has reported that vitamin E benefits in patients with mild to moderate AD were seen by slowing functional decline [119]. Vitamin E lowered the oxidation of blood glutathione and the peroxidation of plasma lipids that cause an improvement in AD. In vivo studies, vitamin E has been shown to prevent the toxic effects of Aβ and improve cognitive performance [62-64]. In the Chicago Health and Aging Project, higher intakes of vitamin E from natural sources were associated with decline in Alzheimer's disease incidence [120]. Similarly, in the Rotterdam study, high vitamin E intake was associated with reduced the incidence of dementia [63]. Furthermore, Dias-Santagataet et al. [121] reported that α-tocopherol administration significantly prevented tau-induced neurotoxicity in Drosophila, and similar beneficial outcomes were recently reported by other researchers using tau pathology in transgenic mouse model [65], which underscored the therapeutic value of vitamin E. However, vitamin E should come from foods, rather than supplements, where, vitamin E from supplements has not been shown to reduce AD risk [122]. Mechanistically, the potential effect of vitamin E in AD is remain elusive, however, vitamin E may exert this potential by preventing Aβ-induced ROS, protecting against oxidation-mediated decline in neurotransmission-associated protein, inhibiting inflammatory cytokines those participated in neuroinflammation and activating PP2A.


Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease
Chemical structure of α-tocopherol form of vitamin E (C29H50O2).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 8: Chemical structure of α-tocopherol form of vitamin E (C29H50O2).
Mentions: There are two groups of vitamin E with different ten forms; five as tocotrienols and five as tocopherols and identified by α-, β-, γ-, δ- and ε-. The most biologically active form of vitamin E is α-tocopherol (Fig. 8). The work of Sano et al. [118] gave impetus to the idea of vitamin E as the treatment of AD. At the present days, the same group has reported that vitamin E benefits in patients with mild to moderate AD were seen by slowing functional decline [119]. Vitamin E lowered the oxidation of blood glutathione and the peroxidation of plasma lipids that cause an improvement in AD. In vivo studies, vitamin E has been shown to prevent the toxic effects of Aβ and improve cognitive performance [62-64]. In the Chicago Health and Aging Project, higher intakes of vitamin E from natural sources were associated with decline in Alzheimer's disease incidence [120]. Similarly, in the Rotterdam study, high vitamin E intake was associated with reduced the incidence of dementia [63]. Furthermore, Dias-Santagataet et al. [121] reported that α-tocopherol administration significantly prevented tau-induced neurotoxicity in Drosophila, and similar beneficial outcomes were recently reported by other researchers using tau pathology in transgenic mouse model [65], which underscored the therapeutic value of vitamin E. However, vitamin E should come from foods, rather than supplements, where, vitamin E from supplements has not been shown to reduce AD risk [122]. Mechanistically, the potential effect of vitamin E in AD is remain elusive, however, vitamin E may exert this potential by preventing Aβ-induced ROS, protecting against oxidation-mediated decline in neurotransmission-associated protein, inhibiting inflammatory cytokines those participated in neuroinflammation and activating PP2A.

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.