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dc.contributor.authorMorales Pérez, Ingrid 
dc.contributor.authorRodríguez, Manuel 
dc.contributor.authorRodríguez Sabaté, Clara
dc.contributor.authorSánchez, Alberto
dc.contributor.authorSabaté, Magdalena
dc.contributor.otherCiencias Médicas Básicas
dc.contributor.otherGrupo de Neurobiología y Neurología Experimental
dc.date.accessioned2024-07-29T20:08:02Z
dc.date.available2024-07-29T20:08:02Z
dc.date.issued2015
dc.identifier.urihttp://riull.ull.es/xmlui/handle/915/38595
dc.description.abstractIt is generally considered that Parkinson’s disease is induced by specific agents that degenerate a clearly defined population of dopaminergic neurons. Data commented in this review suggest that this assumption is not as clear as is often thought and that aging may be critical for Parkinson’s disease. Neurons degenerating in Parkinson’s disease also degenerate in normal aging, and the different agents involved in the etiology of this illness are also involved in aging. Senescence is a wider phenomenon affecting cells all over the body, whereas Parkinson’s disease seems to be restricted to certain brain centers and cell populations. However, reviewed data suggest that Parkinson’s disease may be a local expression of aging on cell populations which, by their characteristics (high number of synaptic terminals and mitochondria, unmyelinated axons, etc.), are highly vulnerable to the agents promoting aging. The development of new knowledge about Parkinson’s disease could be accelerated if the research on aging and Parkinson’s disease were planned together, and the perspective provided by gerontology gains relevance in this field.en
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.relation.ispartofseriesAging Cell (2015) 14
dc.rightsLicencia Creative Commons (Reconocimiento-No comercial-Sin obras derivadas 4.0 Internacional)
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es_ES
dc.titleParkinson's disease as a result of agingen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1111/acel.12312
dc.subject.keywordagingen
dc.subject.keyworddopamineen
dc.subject.keywordnigrostriatal neuronsen
dc.subject.keywordneurodegenerationen
dc.subject.keywordParkinson’s diseaseen


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