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dc.rights.licenseCC-BY-NC-ND
dc.contributor.advisorvan den Berge, S.
dc.contributor.authorBruinsma, I.J.
dc.date.accessioned2010-08-27T17:00:29Z
dc.date.available2010-08-27
dc.date.available2010-08-27T17:00:29Z
dc.date.issued2010
dc.identifier.urihttps://studenttheses.uu.nl/handle/20.500.12932/5387
dc.description.abstractParkinson’s disease is a common neurodegenerative disorder with a high prevalence in people over 65. Its main hallmark is progressive loss of dopaminergic neurons in the substantia nigra, leading to characteristic motor symptoms such as tremor and bradykinesia. The pathology of this disease is not yet fully understood. Recently it has been suggested that astrocytes might play an important role in disease initiation and progression. In response to neuronal damage astrocytes can enter a state called reactive astrogliosis, which is characterised by hypertrophy and increased expression of glial fibrillary acidic protein. Though initially meant as a protective reaction, this can have both beneficial and detrimental effects on surrounding neurons. In this review the role that astrocytes might play in Parkinson’s disease is discussed. Evidence of astrogliosis in animal models of Parkinson’s disease and post mortem studies of patients is described, implicating the involvement of this process. Subsequently, several factors are discussed that are important during the astrocytic response in Parkinson’s disease, divided in neuroprotective and neurodegenerative effects. Based upon the astrocytic factors that could contribute to disease pathology, some potential therapies for Parkinson’s disease targeting astrocytes are suggested.
dc.description.sponsorshipUtrecht University
dc.format.extent1612382 bytes
dc.format.mimetypeapplication/msword
dc.language.isoen
dc.titleAstrocytes in Parkinson's disease
dc.type.contentMaster Thesis
dc.rights.accessrightsOpen Access
dc.subject.keywordsastrocytes, astrogliosis, Parkinson's disease, neuroprotective & neurodegenerative effects
dc.subject.courseuuNeuroscience and Cognition


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