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dc.contributor.authorJurado-Coronel J.C.
dc.contributor.authorÁvila-Rodriguez M.
dc.contributor.authorEcheverria V.
dc.contributor.authorHidalgo O.A.
dc.contributor.authorGonzalez J.
dc.contributor.authorAliev G.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:21:03Z
dc.date.available2020-09-02T22:21:03Z
dc.date.issued2016
dc.identifier10.2174/1871527315666160202125519
dc.identifier.citation15, 3, 292-300
dc.identifier.issn18715273
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4988
dc.descriptionGreen tea is a beverage consumed around the world that is believed to have substantial health benefits such as reducing the risk of cancer, cardiovascular diseases, diabetes and neurodegeneration. This beverage is prepared from the leaves (steamed and dried) of the Camellia sinesis plant and contains strong antioxidant and neuroprotective phenolic compounds from which the most important is (-)-Epigallocatechin-3-gallate. Parkinson’s disease (PD) is the second more common neurodegenerative disorders, after Alzheimer’s disease and is characterized by degeneration of dopaminergic neurons in the pars compact of the substantia nigra of the basal ganglia. It has been shown in pre-clinical and clinical studies that green tea may be able to prevent PD, but its optimal dose or a possible mechanism explaining its health benefit in PD has not been properly established. In this review, we discuss the potential role of green tea’s phenolic compounds and their therapeutic effectin modulating key signaling pathways in the PD brain. © 2016 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers
dc.subject(-)-epigallocatechin-3-gallate
dc.subjectAntioxidant
dc.subjectGreen tea
dc.subjectNeuroprotection
dc.subjectOxidative stress
dc.subjectParkinson disease
dc.subject1 methyl 4 phenylpyridinium
dc.subjectalpha synuclein
dc.subjectamine oxidase (flavin containing) isoenzyme B
dc.subjectamyloid beta protein
dc.subjectcatechin
dc.subjectcatechol methyltransferase
dc.subjectepigallocatechin gallate
dc.subjectFas antigen
dc.subjectFas ligand
dc.subjectgrowth arrest and DNA damage inducible protein 45
dc.subjectheat shock protein 90
dc.subjecthypoxia inducible factor 1alpha
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 1beta
dc.subjectiron
dc.subjectlevodopa
dc.subjectmitogen activated protein kinase
dc.subjectoxidopamine
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprocollagen proline 2 oxoglutarate 4 dioxygenase
dc.subjectprotein BAD
dc.subjectprotein kinase C
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide dehydrogenase
dc.subjectrotenone
dc.subjecttumor necrosis factor alpha
dc.subjecttumor necrosis factor related apoptosis inducing ligand
dc.subjectubiquitin conjugating enzyme E2
dc.subjectunindexed drug
dc.subjectcatechin
dc.subjectneuroprotective agent
dc.subjecttea
dc.subjectaging
dc.subjectantioxidant activity
dc.subjectapoptosis
dc.subjectArticle
dc.subjectbioavailability
dc.subjectCamellia sinensis
dc.subjectcell viability
dc.subjectclinical examination
dc.subjectdisease course
dc.subjectdisorders of mitochondrial functions
dc.subjectenzyme activity
dc.subjectenzyme inhibition
dc.subjecthuman
dc.subjectlipid peroxidation
dc.subjectmetabolism
dc.subjectnervous system inflammation
dc.subjectneuroprotection
dc.subjectneurotoxicity
dc.subjectnonhuman
dc.subjectnuclear magnetic resonance imaging
dc.subjectoxidative stress
dc.subjectParkinson disease
dc.subjectprotein binding
dc.subjectprotein expression
dc.subjecttea
dc.subjectanalogs and derivatives
dc.subjectanimal
dc.subjectchemistry
dc.subjectParkinson disease
dc.subjecttea
dc.subjectAnimals
dc.subjectCatechin
dc.subjectHumans
dc.subjectNeuroprotective Agents
dc.subjectParkinson Disease
dc.subjectTea
dc.titleImplication of green tea as a possible therapeutic approach for Parkinson disease
dc.typeArticle


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