Alzheimer's Disease and Green Tea: Epigallocatechin-3-Gallate as a Modulator of Inflammation and Oxidative Stress

Alzheimer's disease (AD) is the most common cause of dementia, characterised by a marked decline of both memory and cognition, along with pathophysiological hallmarks including amyloid beta peptide (Aβ) accumulation, tau protein hyperphosphorylation, neuronal loss and inflammation in the brain....

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Main Authors: Víctor Valverde-Salazar (Author), Daniel Ruiz-Gabarre (Author), Vega García-Escudero (Author)
Format: Book
Published: MDPI AG, 2023-07-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Víctor Valverde-Salazar  |e author 
700 1 0 |a Daniel Ruiz-Gabarre  |e author 
700 1 0 |a Vega García-Escudero  |e author 
245 0 0 |a Alzheimer's Disease and Green Tea: Epigallocatechin-3-Gallate as a Modulator of Inflammation and Oxidative Stress 
260 |b MDPI AG,   |c 2023-07-01T00:00:00Z. 
500 |a 10.3390/antiox12071460 
500 |a 2076-3921 
520 |a Alzheimer's disease (AD) is the most common cause of dementia, characterised by a marked decline of both memory and cognition, along with pathophysiological hallmarks including amyloid beta peptide (Aβ) accumulation, tau protein hyperphosphorylation, neuronal loss and inflammation in the brain. Additionally, oxidative stress caused by an imbalance between free radicals and antioxidants is considered one of the main risk factors for AD, since it can result in protein, lipid and nucleic acid damage and exacerbate Aβ and tau pathology. To date, there is a lack of successful pharmacological approaches to cure or even ameliorate the terrible impact of this disease. Due to this, dietary compounds with antioxidative and anti-inflammatory properties acquire special relevance as potential therapeutic agents. In this context, green tea, and its main bioactive compound, epigallocatechin-3-gallate (EGCG), have been targeted as a plausible option for the modulation of AD. Specifically, EGCG acts as an antioxidant by regulating inflammatory processes involved in neurodegeneration such as ferroptosis and microglia-induced cytotoxicity and by inducing signalling pathways related to neuronal survival. Furthermore, it reduces tau hyperphosphorylation and aggregation and promotes the non-amyloidogenic route of APP processing, thus preventing the formation of Aβ and its subsequent accumulation. Taken together, these results suggest that EGCG may be a suitable candidate in the search for potential therapeutic compounds for neurodegenerative disorders involving inflammation and oxidative stress, including Alzheimer's disease. 
546 |a EN 
690 |a Alzheimer's disease 
690 |a EGCG 
690 |a neuroprotection 
690 |a antioxidant 
690 |a green tea 
690 |a amyloid β 
690 |a Therapeutics. Pharmacology 
690 |a RM1-950 
655 7 |a article  |2 local 
786 0 |n Antioxidants, Vol 12, Iss 7, p 1460 (2023) 
787 0 |n https://www.mdpi.com/2076-3921/12/7/1460 
787 0 |n https://doaj.org/toc/2076-3921 
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