(−)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer׳s disease model mice by upregulating neprilysin expression

Chang, Xiang; Rong, Cuiping; Chen, Yunbo; Yang, Cong; Hu, Qian; Mo, Yousheng; Zhang, Chunxia; Gu, Xiaoqiong; Zhang, Lei; He, Wen-Qing; Cheng, Shirley; Hou, Xian‐Geng; Su, Ruyu; Liu, Sijun; Dun, Wenjun; Wang, Qi; Fang, Shuhuan

doi:10.1016/j.yexcr.2015.04.004

Cited by 96 publications

(56 citation statements)

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“…A recent study conducted by Chesser et al , proved that EGCG in DIV8 primary rat cortical neurons, was able to enhance the clearance of AD-relevant phosphorylated tau species, indicating that EGCG could be used as an adjuvant agent for AD’s treatment [27]. Similar findings were obtained by Chang et al The authors demonstrated that EGCG reduced β-amyloid (Aβ) accumulation in M146 L and CHO cells [28]. Finally, very recently it has been reported that EGCG inhibited β-Amyloid generation and oxidative stress involvement of nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) in N2a/APP695 cells [29].…”

Section: Introductionmentioning

confidence: 62%

“…The authors showed that EGCG attenuated the cognitive deterioration in AD’s mouse model by upregulation of neprilysin (NEP) expression [28]. Taken together, these data strongly suggest that EGCG could be used as a therapeutic agent for the treatment and the prevention of AD. …”

Section: Introductionmentioning

confidence: 99%

“…ICV infusion of STZ (3 mg/kg)EGCG completely abrogated the cognitive deficit, S100B content in the hippocampus, AChE activity, glutathione peroxidase activity, NO metabolites, and ROS content[34] ICR mice model of systemic inflammation 1.5 and 3 mg/kg for 3 weeks (Oral gavage). LPS (250 μg/kg) intraperitonealEGCG prevented LPS-induced memory impairment, apoptotic neuronal cell death, and microglia activation[19] AD mouse model induced by D-gal 2 mg/(kg/ day) or 6 mg/(kg/day) for 4 weeks, oral gavageEGCG decreased the expression of APP and beta-Amyloid in the hippocampus of mice.[35] APP/PS1 mice 2 mg/(kg/day) or 6 mg/(kg/day) for 4 weeks, oral gaveEGCG treatment inhibited TNF-α/JNK signaling, increased the phosphorylation of Akt and glycogen synthase kinase-3β.[37] SAMP8 mice 5 and 15 mg/kg, for 60 days, intragastricEGCG induced reduction in Aβ accumulation and increased NEP expression[28] …”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice

Cascella

Bimonte

Muzio³

et al. 2017

Infect Agents Cancer

119

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Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia characterized by cognitive and memory impairment. One of the mechanism involved in the pathogenesis of AD, is the oxidative stress being involved in AD‘s development and progression. In addition, several studies proved that chronic viral infections, mainly induced by Human herpesvirus 1 (HHV-1), Cytomegalovirus (CMV), Human herpesvirus 2 (HHV-2), and Hepatitis C virus (HCV) could be responsible for AD’s neuropathology. Despite the large amount of data regarding the pathogenesis of Alzheimer’s disease (AD), a very limited number of therapeutic drugs and/or pharmacological approaches, have been developed so far. It is important to underline that, in recent years, natural compounds, due their antioxidants and anti-inflammatory properties have been largely studied and identified as promising agents for the prevention and treatment of neurodegenerative diseases, including AD. The ester of epigallocatechin and gallic acid, (−)-Epigallocatechin-3-Gallate (EGCG), is the main and most significantly bioactive polyphenol found in solid green tea extract. Several studies showed that this compound has important anti-inflammatory and antiatherogenic properties as well as protective effects against neuronal damage and brain edema. To date, many studies regarding the potential effects of EGCG in AD’s treatment have been reported in literature. The purpose of this review is to summarize the in vitro and in vivo pre-clinical studies on the use of EGCG in the prevention and the treatment of AD as well as to offer new insights for translational perspectives into clinical practice.

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Section: Introductionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice

Cascella

Bimonte

Muzio³

et al. 2017

Infect Agents Cancer

119

View full text Add to dashboard Cite

show abstract

“…[14][15][16] Studies showed epigenetic linkage of aging, cancer, and nutrition. 17,18 Histone deacetylase inhibitors have been proven to be important key targets in cancer therapy and also have attracted significant attention to treating neurodegenerative disorders recently. [18][19][20][21][22] Our previous studies found EGCG as an HDACi could inhibit the growth of adrenal pheochromocytoma, meanwhile, its neuroprotective effect was also confirmed in the AD model both in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Histone Deacetylase and Amyloid Precursor Protein in Hepatocellular Carcinoma

Zhao

Jiao

et al. 2016

Technol Cancer Res Treat

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Epigenetic modifications are involved in the pathogenesis of cancer, and histone deacetylase inhibitors are considered potential therapeutic agents. Histone tails undergo acetylation at lysine residues, which is associated with transcriptional activation. However, previous studies indicated that as histone deacetylase inhibitors, both (À)-epigallocatechin-3-gallate and valproic acid presented the effects of downregulation of amyloid precursor protein expression, which resulted in the induction of apoptosis. The downregulation of amyloid precursor protein, instead of conventionally activating gene expression as histone deacetylase inhibitor, was attractive. However, there was no relevant report on the correlation of the expression of amyloid precursor protein and histone deacetylase 1 in cancer. In the present study, we detected the expression of amyloid precursor protein and histone deacetylase 1 in hepatocellular carcinoma and adjacent tissues, as well as the correlations among histone deacetylase 1, amyloid precursor protein, and tumor stage. The results showed that the expressions of amyloid precursor protein and histone deacetylase 1 were significantly higher in hepatocellular carcinoma tissues than that in adjacent tissues (P < .05), however, there was no statistical difference between amyloid precursor protein and histone deacetylase 1 with tumor stages. The present findings provided more foundation for the study on amyloid precursor protein metabolism in cancer, especially on the regulation of amyloid precursor protein by histone deacetylases.

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“…EGCG has efects on learning and memory [47] that may be useful in the treatment of Alzheimer's disease [48]. It has also been suggested for Parkinson's disease therapy [49] while some novel EGCG derivatives may be useful for neuropathic pain [50].…”

Section: (−)-Epigallocatechin Gallate (Egcg)mentioning

confidence: 99%

Flavonoid Actions on Receptors for the Inhibitory Neurotransmitter GABA

Hinton¹,

Hanrahan²,

Johnston³

2017

Flavonoids - From Biosynthesis to Human Health

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Flavonoids, both naturally occurring and synthetic, are known to have multiple efects on the activation of ionotropic receptors for γ-aminobutyric acid (GABA), the major inhibitory neurotransmiter in our brains. They can act as positive or negative allosteric modulators, enhancing or reducing the efect of GABA. They can elicit a direct activation of the receptors. They can also act to modulate the action of other modulators. This ability to inluence function via their actions on GABA receptors permits a range of efects of lavonoids, including relief of anxiety, anticonvulsant, analgesic and sedative actions.

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(−)-Epigallocatechin-3-gallate attenuates cognitive deterioration in Alzheimer׳s disease model mice by upregulating neprilysin expression

Cited by 96 publications

References 50 publications

The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice

The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice

Overexpression of Histone Deacetylase and Amyloid Precursor Protein in Hepatocellular Carcinoma

Flavonoid Actions on Receptors for the Inhibitory Neurotransmitter GABA

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