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Abstract
The potential to treat neurodegenerative diseases (NDs) of the major bioactive compound of green tea, epigallocatechin-3-gallate (EGCG), is well documented. Numerous findings now suggest that EGCG targets protein misfolding and aggregation, a common cause and pathological mechanism in many NDs. Several studies have shown that EGCG interacts with misfolded proteins such as amyloid beta-peptide (Aβ), linked to Alzheimer’s disease (AD), and α-synuclein, linked to Parkinson’s disease (PD). To date, NDs constitute a serious public health problem, causing a financial burden for health care systems worldwide. Although current treatments provide symptomatic relief, they do not stop or even slow the progression of these devastating disorders. Therefore, there is an urgent need to develop effective drugs for these incurable ailments. It is expected that targeting protein misfolding can serve as a therapeutic strategy for many NDs since protein misfolding is a common cause of neurodegeneration. In this context, EGCG may offer great potential opportunities in drug discovery for NDs. Therefore, this review critically discusses the role of EGCG in NDs drug discovery and provides updated information on the scientific evidence that EGCG can potentially be used to treat many of these fatal brain disorders.
Highlights
Neurodegenerative diseases (NDs) are a global public health threat and a huge financial burden for health care systems, not to mention a major hardship for society and families [1,2,3]
A considerable body of evidence that supports the use of EGCG for ND therapy has become available over the past two decades
The potential effects of EGCG in NDs are well described and proven by a range of experimental in vitro and in vivo assays discussed in this review
Summary
Neurodegenerative diseases (NDs) are a global public health threat and a huge financial burden for health care systems, not to mention a major hardship for society and families [1,2,3]. EGCG is a dietary polyphenol found in green tea with potent antioxidant and anti-inflammatory effects and an ability to modulate multiple targets implicated in the pathogenesis of many chronic diseases, including cancer, cardiovascular diseases, diabetes, and NDs [12]. The pathogenesis of NDs shares many fundamental processes associated with progressive neuronal dysfunction and death, with protein misfolding, oxidative stress, apoptosis, and neuroinflammation as some of them [14,15]. Each ND is associated with abnormalities in the folding of a different protein, the molecular pathways leading to misfolding and aggregation appear to be similar. These findings suggest that a common therapy for NDs might be possible [24].
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