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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 Ellagic acid (C14H6O8), punicalagin (C48H28O30), punicalin (C34H22O22) and epigallocatechin-3-gallate (C22H18O11).
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Figure 5: Chemical structures of Ellagic acid (C14H6O8), punicalagin (C48H28O30), punicalin (C34H22O22) and epigallocatechin-3-gallate (C22H18O11).

Mentions: Punica granatum (pomegranate) has the potential to suppress the AD pathogenic cascade at multiple sites. Pomegranate juice decreased amyloid load and improved behavior in APPsw (double Swedish APP mutation; Tg2576) transgenic mouse model of AD [61]. Ellagic acid, punicalagin and punicalin (Fig. 5) of pomegranate were found to be powerful β-secretace inhibitors [60]. Also, pomegranate shows a direct radical scavenging activity with lipid peroxidation inhibiting property, particularly metal catalyzed peroxidation [103]. Pomegranate is also known as a good inhibitor of gene expression of inflammatory cytokines such as IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2), COX-2, and iNOS by influence of inhibition of JUN and NF-κB-mediated gene transcription [104-105]. All of these inflammatory cytokines have been implicated in Aβ toxicity, indicating the multi-target intervention of pomegranate in AD. In addition, pomegranate polyphenols attenuate disruption of mitochondrial membrane [106]. Furthermore, pomegranate has other proven anti-amyloid activities. Pomegranate decreased soluble Aβ levels and Aβ deposition by inhibiting BACE1 [60]. Ellagic acid, a phenol found abundantly in pomegranate inhibits Aβ plaques formation and Aβ toxicity in vitro [107]. Another polyphenol found in pomegranate, epigallocatechin-3-gallate (EGCG; Fig. 5), reduces Aβ formation and Aβ plaques deposition in the brain of transgenic mouse containing the human Swedish APP mutation [61]. This anti-amyloid activity of pomegranate remains effective in aged mice, even after amyloid deposition continues over time. Interestingly, pomegranate was shown to decrease Aβ plaques load and improve memory impairment in behavioral performance testes in AD transgenic mice [108] even in response to acute Aβ brain injection [109].


Oxidant/Antioxidant Imbalance and the Risk of Alzheimer's Disease
Chemical structures of Ellagic acid (C14H6O8), punicalagin (C48H28O30), punicalin (C34H22O22) and epigallocatechin-3-gallate (C22H18O11).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Chemical structures of Ellagic acid (C14H6O8), punicalagin (C48H28O30), punicalin (C34H22O22) and epigallocatechin-3-gallate (C22H18O11).
Mentions: Punica granatum (pomegranate) has the potential to suppress the AD pathogenic cascade at multiple sites. Pomegranate juice decreased amyloid load and improved behavior in APPsw (double Swedish APP mutation; Tg2576) transgenic mouse model of AD [61]. Ellagic acid, punicalagin and punicalin (Fig. 5) of pomegranate were found to be powerful β-secretace inhibitors [60]. Also, pomegranate shows a direct radical scavenging activity with lipid peroxidation inhibiting property, particularly metal catalyzed peroxidation [103]. Pomegranate is also known as a good inhibitor of gene expression of inflammatory cytokines such as IL-6, IL-8, vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2), COX-2, and iNOS by influence of inhibition of JUN and NF-κB-mediated gene transcription [104-105]. All of these inflammatory cytokines have been implicated in Aβ toxicity, indicating the multi-target intervention of pomegranate in AD. In addition, pomegranate polyphenols attenuate disruption of mitochondrial membrane [106]. Furthermore, pomegranate has other proven anti-amyloid activities. Pomegranate decreased soluble Aβ levels and Aβ deposition by inhibiting BACE1 [60]. Ellagic acid, a phenol found abundantly in pomegranate inhibits Aβ plaques formation and Aβ toxicity in vitro [107]. Another polyphenol found in pomegranate, epigallocatechin-3-gallate (EGCG; Fig. 5), reduces Aβ formation and Aβ plaques deposition in the brain of transgenic mouse containing the human Swedish APP mutation [61]. This anti-amyloid activity of pomegranate remains effective in aged mice, even after amyloid deposition continues over time. Interestingly, pomegranate was shown to decrease Aβ plaques load and improve memory impairment in behavioral performance testes in AD transgenic mice [108] even in response to acute Aβ brain injection [109].

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.