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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 vitamin B12 (C63H88CoN14O14P).
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Figure 9: Chemical structure of vitamin B12 (C63H88CoN14O14P).

Mentions: Vitamin B12 (Fig. 9) is essential for the health of the brain and nervous system and for blood cell formation [123]. However, vitamin B12 is lowered in elderly adults especially in males. Moore et al. [124] showed that low serum levels of vitamin B12 are allied with neurodegenerative disease and cognitive impairment and that vitamin B12 therapy does not improve cognition in patients without preexisting deficiency. Vitamin B12 supplementation increased the activity of choline acetyltransferase in cholinergic neurons in cats [66] and improved cognitive performance in AD patients possibly by its ability to reduce homocysteine levels [125]. Hyperhomocysteinemia was implicated in neurotoxicity by overstimulation of NMDA receptors or by increasing the vulnerability of hippocampal neurons to excitotoxicity and Aβ toxicity.


Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease
Chemical structure of vitamin B12 (C63H88CoN14O14P).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 9: Chemical structure of vitamin B12 (C63H88CoN14O14P).
Mentions: Vitamin B12 (Fig. 9) is essential for the health of the brain and nervous system and for blood cell formation [123]. However, vitamin B12 is lowered in elderly adults especially in males. Moore et al. [124] showed that low serum levels of vitamin B12 are allied with neurodegenerative disease and cognitive impairment and that vitamin B12 therapy does not improve cognition in patients without preexisting deficiency. Vitamin B12 supplementation increased the activity of choline acetyltransferase in cholinergic neurons in cats [66] and improved cognitive performance in AD patients possibly by its ability to reduce homocysteine levels [125]. Hyperhomocysteinemia was implicated in neurotoxicity by overstimulation of NMDA receptors or by increasing the vulnerability of hippocampal neurons to excitotoxicity and Aβ toxicity.

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.