Green tea polyphenols protect against okadaic acid-induced acute learning and memory impairments in rats

Li, Hongyu; Wu, Xiukui; Wu, Qiong; Gong, Daozhi; Shi, Meijun; Guan, Lili; Zhang, Jun; Liu, Jing; Yuan, Bo; Han, Guozhu; Zou, Yuan

doi:10.1016/j.nut.2013.08.021

Cited by 23 publications

(16 citation statements)

References 32 publications

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“…All these compounds show excellent antioxidant activities and beneficial effects in preventing oxidative stress, mitochondrial dysfunction and inflammation in the experimental models of neurodegenerative disorders (Calabrese et al, 2012; Lee et al, 2015; Li et al, 2014; Nataraj et al, 2015; Rege et al, 2013; Singhal et al, 2013; Subash et al, 2014a, 2014b, 2015; Tapias et al, 2014; Vauzour, 2012; Vepsäläinen et al, 2013; Wang et al, 2014]. One of the well-known polyphenols is resveratrol (3, 5, 4’-trihydroxy-trans-stilbene) contained in red grapes and it has been shown to protect the brain from oxidative damage (Gacar et al, 2011).…”

Section: Translational Research Opportunities and Challengesmentioning

confidence: 99%

“…One of the well-known polyphenols is resveratrol (3, 5, 4’-trihydroxy-trans-stilbene) contained in red grapes and it has been shown to protect the brain from oxidative damage (Gacar et al, 2011). In addition, the green tea polyphenols have been shown to inhibit amyloid fibril formation, protects neurons from oxidative damage caused by Aβ in AD, decrease hyper-phosphorylated Tau, and ameliorate primary hippocampal neuronal damage induced by okadaic acid (Li et al, 2014). Similarly, polyphenols from pomegranate juice have been shown to inhibit rotenone-induced inflammation and neurodegeneration in AD and PD animal models (Tapias et al, 2014).…”

Section: Translational Research Opportunities and Challengesmentioning

confidence: 99%

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Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities.

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Section: Translational Research Opportunities and Challengesmentioning

confidence: 99%

Section: Translational Research Opportunities and Challengesmentioning

confidence: 99%

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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“…Green tea polyphenols protected against okadaic acid-induced acute learning and memory impairments in rats [290].…”

Section: Natural Productsmentioning

confidence: 98%

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Froestl

Pfeifer

Muhs

2014

JAD

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Scientists working in the field of Alzheimer's disease and, in particular, cognitive enhancers, are very productive. The review "Drugs interacting with Targets other than Receptors or Enzymes. Disease-modifying Drugs" was accepted in October 2012. In the last 20 months, new targets for the potential treatment of Alzheimer's disease were identified. Enormous progress was realized in the pharmacological characterization of natural products with cognitive enhancing properties. This review covers the evolution of research in this field through May 2014.

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“…The results indicated that potential biomarkers, including LPC 16:0, LPC 18:2, LPC 18:0, LPC 20:5, LPC 20:4, LPC 22:6, tryptophan, dihydrosphingosine, and phytosphingosine were identified for aging rats and that the GTPs can reverse these irregularities, which are related to the perturbations in lecithin, amino acid, and phospholipid metabolism . Many studies have reported that either GTP or EGCG has antiapoptotic, antioxidative, and anti‐inflammatory effects, suggesting that these compounds may be useful in disease‐modifying treatments for AD …”

Section: Metabolomics: a Tool For Understanding Natural Drugs Against Admentioning

confidence: 99%

“…44 Many studies have reported that either GTP or EGCG has antiapoptotic, antioxidative, and anti-inflammatory effects, suggesting that these compounds may be useful in disease-modifying treatments for AD. 51 Kai-Xin-San (KXS) is a classic and major TCM herbal formula containing the following herbs: radix ginseng (dried root or rhizome of P. ginseng C. A. Mey.…”

Section: Lc-ms-based Metabolomicsmentioning

confidence: 99%

Characterizing Alzheimer's disease through metabolomics and investigating anti‐Alzheimer's disease effects of natural products

Liu

Wang

et al. 2017

Annals of the New York Academy of Sciences

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Alzheimer's disease (AD) is the most common cause of dementia in elderly people and is among the greatest healthcare challenges of the 21st century. However, the etiology and pathogenesis of AD remain poorly understood, and no curative treatments are available to slow down or stop the degenerative effects of AD. As a high-throughput approach, metabolomics is gaining significant attention in AD research, because it has a powerful potential to discover novel biomarkers, unravel new therapeutic targets for AD, and identify perturbed metabolic pathways involved in AD progression. Here, we systematically review metabolomics with regard to its recent advances and applications in the identification of potential biomarkers for early AD diagnosis and pathogenesis research. In addition, we illustrate the developments in metabolomics as an effective tool for understanding the anti-AD mechanisms of natural products. We believe that the insights from these advances can narrow the gap between metabolomics research and clinical applications of laboratory findings. Moreover, we discuss some limitations and perspectives of biomarker identification in metabolomics.

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Green tea polyphenols protect against okadaic acid-induced acute learning and memory impairments in rats

Cited by 23 publications

References 32 publications

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Characterizing Alzheimer's disease through metabolomics and investigating anti‐Alzheimer's disease effects of natural products

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