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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 structures of β-carotene (C40H56) and 1,25Dihydroxy-vitamin D3 (C27H40O).
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Figure 10: Chemical structures of β-carotene (C40H56) and 1,25Dihydroxy-vitamin D3 (C27H40O).

Mentions: A relationship between dietary carotenoids and age-related cognitive function has been reported. Perrig et al. [126] noted that the higher level of β-carotene in plasma was associated with better memory performances (priming, working-memory, free recall, recognition and vocabulary test) in old and very old subjects. β-Carotene (a major precursor to vitamin A; Fig. 10) might have beneficial effects via its antioxidant or Aβ anti-oligomerisation effects [127-128]. Certain carotenoids also may modulate the functional properties of synaptic membranes [128], enhance gap junctional communication [67].


Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease
Chemical structures of β-carotene (C40H56) and 1,25Dihydroxy-vitamin D3 (C27H40O).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 10: Chemical structures of β-carotene (C40H56) and 1,25Dihydroxy-vitamin D3 (C27H40O).
Mentions: A relationship between dietary carotenoids and age-related cognitive function has been reported. Perrig et al. [126] noted that the higher level of β-carotene in plasma was associated with better memory performances (priming, working-memory, free recall, recognition and vocabulary test) in old and very old subjects. β-Carotene (a major precursor to vitamin A; Fig. 10) might have beneficial effects via its antioxidant or Aβ anti-oligomerisation effects [127-128]. Certain carotenoids also may modulate the functional properties of synaptic membranes [128], enhance gap junctional communication [67].

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.