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dc.contributor.authorJurado-Coronel J.C.
dc.contributor.authorÁvila-Rodriguez M.
dc.contributor.authorCapani F.
dc.contributor.authorGonzalez J.
dc.contributor.authorMorán V.E.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:21:03Z
dc.date.available2020-09-02T22:21:03Z
dc.date.issued2016
dc.identifier10.2174/138161282210160304112133
dc.identifier.citation22, 10, 1305-1311
dc.identifier.issn13816128
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4987
dc.descriptionParkinson’s disease (PD) is a relatively common disorder of the Central Nervous System (CNS), whose etiology is characterized by a selective and progressive degeneration of dopaminergic neurons, and the presence of Lewy bodies in the pars compacta of the substantia nigra, and gaping dopamine depletion in the striatum. Patients with this disease suffer from tremors, slowness of movements, gait instability, and rigidity. These patients may also present functional disability, reduced quality of life, and rapid cognitive decline. It has been shown that nicotine exerts beneficial effects in patients with PD and in in-vitro and in-vivo models of this disease. Astrocytes are an important component in the immune response associated with PD, and that nicotine might be able to inhibit the inflammation-related apoptosis of these cells, being this a potential strategy for PD treatment. This action of nicotine could be due mainly to activation of α7 nicotinic acetylcholine receptors (α7-nAChRs) expressed in glial cells. However, nicotine administration can protect dopaminergic neurons against degeneration by inhibiting astrocytes activation in the substantia nigra pars compacta (SNpc) and therefore reduce inflammation. Owing to the toxicity and capacity of nicotine to induce addiction, analogues of this substance have been designed and tested in various experimental paradigms, and targeting α7-nAChRs expressed in glial cells may be a novel therapeutic strategy for PD treatment. © 2016 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers
dc.subjectApoptosis
dc.subjectAstrocytes
dc.subjectnAChRs
dc.subjectNeuroinflammation
dc.subjectNeuroprotection
dc.subjectNicotine
dc.subjectParkinson disease
dc.subjectnicotine
dc.subjectnicotinic receptor
dc.subjectneuroprotective agent
dc.subjectnicotinic receptor
dc.subjectapoptosis
dc.subjectArticle
dc.subjectastrocyte
dc.subjectcell activation
dc.subjectcognitive defect
dc.subjectdisability
dc.subjectdisease course
dc.subjectdopaminergic nerve cell
dc.subjectdrug mechanism
dc.subjectgait disorder
dc.subjectglia cell
dc.subjecthuman
dc.subjectimmune response
dc.subjectin vitro study
dc.subjectin vivo study
dc.subjectmuscle rigidity
dc.subjectnerve cell plasticity
dc.subjectnervous system inflammation
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectParkinson disease
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein targeting
dc.subjectquality of life
dc.subjectsubstantia nigra pars compacta
dc.subjecttremor
dc.subjectanimal
dc.subjectastrocyte
dc.subjectchemistry
dc.subjectdrug effects
dc.subjectmetabolism
dc.subjectParkinson disease
dc.subjectpathology
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectHumans
dc.subjectNeuroprotective Agents
dc.subjectParkinson Disease
dc.subjectReceptors, Nicotinic
dc.titleTargeting the nicotinic acetylcholine receptors (nAChRs) in astrocytes as a potential therapeutic target in Parkinson’s disease
dc.typeArticle


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