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Review
. 2015;12(4):335-49.
doi: 10.2174/1567205012666150325182702.

Oxidant/Antioxidant imbalance and the risk of Alzheimer's disease

Ahmed E Abdel Moneim  1
Affiliations
Review

Oxidant/Antioxidant imbalance and the risk of Alzheimer's disease

Ahmed E Abdel Moneim. Curr Alzheimer Res. 2015.

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.

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Figures

Fig. (1)
Fig. (1)
Amyloid hypothesis. During AD development, amyloid precursor protein is cleavage to produce β amyloid peptide that aggregates and accumulates to form amyloid-β plaques. This plaques cause neurotoxicity or microglia activation, which in turn microglia release ROS and many pro-inflammatory cytokines such as NO, PGE2, IL-1, IL-6, and TNF-α that accelerate cholinergic neuron damage. These pro-inflammatory cytokines subsequently activate astrocytes that also produce more cytokines to amplify the inflammatory signals and result in neuroinflammation and neurodegeneration.
Fig. (2)
Fig. (2)
Interventions between oxidative stress and the other key factors in AD.
Fig. (3)
Fig. (3)
Chemical structure of melatonin (C13H16N2O2).
Fig. (4)
Fig. (4)
Estrogens chemical structures. 17β-Estradiol (C18H24O2), estrone (C18H22O2) and estriol (C18H24O3).
Fig. (5)
Fig. (5)
Chemical structures of Ellagic acid (C14H6O8), punicalagin (C48H28O30), punicalin (C34H22O22) and epigallocatechin-3-gallate (C22H18O11).
Fig. (6)
Fig. (6)
Chemical structure of S-Allyl-L-Cysteine (C6H11NO2S).
Fig. (7)
Fig. (7)
Chemical structure of silibinin (C25H22O10).
Fig. (8)
Fig. (8)
Chemical structure of α-tocopherol form of vitamin E (C29H50O2).
Fig. (9)
Fig. (9)
Chemical structure of vitamin B12 (C63H88CoN14O14P).
Fig. (10)
Fig. (10)
Chemical structures of β-carotene (C40H56) and 1,25Dihydroxy-vitamin D3 (C27H40O).
Fig. (11)
Fig. (11)
Chemical structure of docosahexaenoic acid (DHA; C22H32O2).
Fig. (12)
Fig. (12)
Chemical structure of coenzyme Q10 (C59H90O4).
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