La maladie de Parkinson au Canada (serveur d'exploration)

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Epigallocatechin-3-Gallate, a Promising Molecule for Parkinson's Disease?

Identifieur interne : 000735 ( Main/Exploration ); précédent : 000734; suivant : 000736

Epigallocatechin-3-Gallate, a Promising Molecule for Parkinson's Disease?

Auteurs : Justine Renaud [Canada] ; Seyed Fazel Nabavi [Iran] ; Maria Daglia [Italie] ; Seyed Mohammad Nabavi [Iran] ; Maria-Grazia Martinoli [Canada]

Source :

RBID : pubmed:25625827

English descriptors

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease, and it is characterized by the loss of the neurotransmitter dopamine and neuronal degeneration in the substantia nigra pars compacta. Thus far, current therapeutic strategies have failed to address neuronal degeneration. It has been reported that overproduction of reactive oxygen species, resulting in oxidative stress, and neuroinflammation play an important role in neurodegenerative diseases through the induction of macromolecular oxidative damage and modulation of intracellular signaling pathways concurring to neuronal cell death. Indeed, anti-oxidant and anti-inflammatory drugs have been the subject of recommendation as a complementary therapy alongside an effective symptomatic treatment to hamper the progression of PD. Today, much attention is paid to polyphenols in light of their potent capacity to reduce oxidative stress and inflammation, while having much fewer side effects than most other drugs. Camellia sinensis L. is the most common ancient herbal tea prepared as a beverage worldwide and it possesses numerous beneficial effects on human health. Epigallocatechin-3-gallate is the best-known bioactive component of C. sinensis and is recognized to exert potent neuroprotective effects against oxidative stress, neuroinflammation, protein aggregation, autophagy, and neuronal cell death in vitro as well as in vivo. The present review appraises the available literature on the beneficial role of epigallocatechin-3-gallate pertaining to dopaminergic degeneration characteristic of PD with particular emphasis on its possible mechanisms of action.

DOI: 10.1089/rej.2014.1639
PubMed: 25625827


Affiliations:


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