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, Marco; Bimonte, Sabrina; Muzio, María Rosaria; Schiavone, Vincenzo; Cuomo, Arturo

doi:10.1186/s13027-017-0145-6

Cited by 129 publications

(76 citation statements)

References 51 publications

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“…Gallic acid is also part of a derivative known as (−)-epigallocatechin gallate (EGCG) ( Table 1) that is a well-known inhibitor of amyloidogenesis. Found in green tea, EGCG has been shown to inhibit other amyloidogenic proteins such as amyloid-beta (Aβ) and tau (both implicated in Alzheimer's disease) [56][57][58]. When incubated with αS, EGCG has been shown to redirect amyloid formation to off-pathway non-toxic aggregates [59].…”

Section: Inhibitors Of αS Amyloidogenesis: What Others Have Discoveredmentioning

confidence: 99%

Pre-structured hydrophobic peptide β-strands: A universal amyloid trap?

Sivanesam¹,

Andersen²

2019

Archives of Biochemistry and Biophysics

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Amyloid fibril formation has long been studied because of the variety of proteins that are capable of adopting this structure despite sharing little sequence homology. This makes amyloid fibrils a challenging focus for inhibition studies because the peptides and proteins that form amyloid fibrils cannot be targeted based on a sequence motif. Most peptide inhibitors that target specific amyloidogenic proteins rely heavily on sequence recognition to ensure that the inhibitory peptide is able to bind its target. This approach is limited to targeting one amyloidogenic protein at a time. However, there is increasing evidence of cross-reactivity between amyloidforming polypeptides. It has therefore become more useful to study the similarities between these proteins that goes beyond their sequence homology. Indeed, the observation that amyloidogenic proteins adopt similar secondary structures along the pathway to fibril formation opens the way to an interesting investigation: the development of inhibitors that could be universal amyloid traps. The review below will analyze two specific amyloidogenic proteins, α-synuclein and human amylin, and introduce a small number of peptides that have been shown to be capable of inhibiting the amyloidogenesis of both of these very dissimilar polypeptides. Some of the inhibitory peptide motifs may indeed, be applicable to Aβ and other amyloidogenic systems.

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Section: Inhibitors Of αS Amyloidogenesis: What Others Have Discoveredmentioning

confidence: 99%

Pre-structured hydrophobic peptide β-strands: A universal amyloid trap?

Sivanesam¹,

Andersen²

2019

Archives of Biochemistry and Biophysics

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“…‐Modulates cerebral blood flow and electroencephalographic activity in RCTs; effects not correlated with improved cognitive functions (Cascella et al, )…”

Section: Phytochemicals As Nutraceuticalsmentioning

confidence: 99%

“…In addition to reducing oxidative stress in an animal model of AD, EGCG also inhibited acetylcholinesterase (AChE) (Howes & Simmonds, ), indicating multiple mechanistic effects relevant to neuroprotection and cholinergic function. EGCG is anti‐inflammatory via different mechanisms and inhibits the neuroinflammatory response of microglia to Aβ (Cascella, Bimonte, Muzio, Schiavone, & Cuomo, ). With respect to AD pathology, EGCG is also a potent inhibitor of β‐ and γ‐secretase activities, with the pyrogalloyl moiety considered essential for activity to prevent Aβ aggregation and to reduce plaque load, effects that improve cognitive functions in vivo (Costa et al, ; Williams et al, ).…”

Section: Phytochemicals As Nutraceuticalsmentioning

confidence: 99%

“…Its antioxidant mechanisms explain its ability to improve memory in many of these studies, including via reduced oxidative damage through enhancing glutathione (GSH) and decreasing lipid peroxide levels in brain tissue Sarker & Franks, 2018;Williams et al, 2011). Animal studies also show curcumin improves memory tasks and it can reverse stress-induced reductions in neurogenesis, associated with brain-derived neurotrophic factor (BDNF; Poulose, Miller, Scott, & Shukitt-Hale, T A B L E 1 Nutraceutical phytochemicals with relevance to cognition in normal and pathological brain ageing EGCG -Antioxidant and neuroprotective against oxidative stress via elevation of mRNA expression of γ-glutamylcysteine ligase to increase cellular GSH, stimulation of PKC and modulation of cell cycle genes (Williams et al, 2011) -Activates α7 nicotinic receptors and signalling molecules P13K and AKT to suppress Bcl-2 down-regulation (Howes & Simmonds, 2014) -Inhibits AChE, is anti-inflammatory via different mechanisms and inhibits neuroinflammatory response of microglia to Aβ (Cascella et al, 2017) -Inhibits βand γ-secretase activities (Costa et al, 2017;Williams et al, 2011) Epicatechin -Increases GSH levels in astrocytes -Improves memory by ameliorating lipid peroxidation and ROS in rats with Aβ-induced hippocampal toxicity (Williams et al, 2011) Cocoa flavanols -Enhance expression of neuroprotective and neuromodulatory proteins (Sokolov et al, 2013) -Improve angiogenesis and cerebral blood flow in the brain (Dominguez & Barbagallo, 2018) Green tea -Epidemiological evidence suggests regular intake reduced age-related cognitive decline and dementia risk (Williams et al, 2011) -Intake (2 g daily for 3 months in an RCT) improved cognitive performance ( affect global cognition or memory (Zhou et al, 2018) Caffeoylquinic acids (including chlorogenic acid)…”

Section: Turmericmentioning

confidence: 99%

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Role of phytochemicals as nutraceuticals for cognitive functions affected in ageing

Howes

Perry²,

Vásquez-Londoño

et al. 2020

British J Pharmacology

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Cognitive decline can occur with normal ageing and in age‐related brain disorders, such as mild cognitive impairment and dementia, including Alzheimer's disease, with limited pharmacological therapies available. Other approaches to reduce cognitive decline are urgently needed, and so, the role of dietary interventions or nutraceuticals has received much attention in this respect. In this review, we examine the evidence for dietary plants and their chemical constituents as nutraceuticals, relevant to both cognitive decline in normal ageing and in dementia. Pharmacological (in vitro and in vivo), clinical and epidemiological evidence is assessed for both frequently consumed plants and their dietary forms, including tea, coffee, cocoa (chocolate), red wine, grapes, citrus and other fruits; in addition to plants used less frequently in certain diets and those that cross the blurred boundaries between foods, nutraceuticals and medicinal plants. For the latter, turmeric, saffron, sage, rosemary and lemon balm are examples of those discussed. Linked Articles This article is part of a themed section on The Pharmacology of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.6/issuetoc

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“…Alzheimer's disease (AD) is a neurodegenerative disorder, its primary character is cognitive impairment and memory impairment . Abnormal expression and accumulation of amyloid β‐peptide (Aβ) in brain tissues are the main causes of AD .…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of mogrol against Aβ1–42-induced memory impairment neuroinflammation and apoptosis in mice

Chen

Liu

Meng

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives Cognitive impairment is the main character of Alzheimer's disease (AD). This study mainly focused on whether mogrol, a tetracyclic triterpenoids compound of Siraitia grosvenorii Swingle, can ameliorate the memory impairment induced by Aβ1–42. Methods Memory impairment mice model was made by stereotactic intra‐hippocampal microinjection of Aβ1–42 (410 pm/mouse). Mogrol (20, 40, 80 mg/kg) was given to mice by intragastric administration at 3 days after Aβ1–42 injection for totally 3 weeks. Morris water maze test and Y‐maze test were operated to evaluate the therapeutic effect of morgrol on Aβ1–42‐induced memory impairments. Immunohistochemical analyses and Hoechst 33258 assay were used to evaluate effect of morgrol on Aβ1–42‐induced microglia overactivation and apoptotic response in hippocampus of mice. Western blotting assay was used to evaluate effect of mogrol on the Aβ1–42‐activated NF‐κB signaling. Key findings Mogrol could significantly alleviate Aβ1–42‐induced memory impairments, inhibit Aβ1–42‐induced microglia overactivation and prevent Aβ1–42‐triggered apoptotic response in the hippocampus. Mogrol also could suppress Aβ1–42‐activated NF‐κB signaling, reduce the production of proinflammatory cytokines. Conclusions This study suggested that mogrol would ameliorate the memory impairment induced by Aβ1–42, which is involved in anti‐inflammation and anti‐apoptosis in the brain.

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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

Cited by 129 publications

References 51 publications

Pre-structured hydrophobic peptide β-strands: A universal amyloid trap?

Pre-structured hydrophobic peptide β-strands: A universal amyloid trap?

Role of phytochemicals as nutraceuticals for cognitive functions affected in ageing

Neuroprotective effect of mogrol against Aβ1–42-induced memory impairment neuroinflammation and apoptosis in mice

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