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dc.rights.licenseCC-BY-NC-ND
dc.contributor.advisorHöppener, Dr J.W.M.
dc.contributor.authorMade, A.M. van der
dc.date.accessioned2011-07-25T17:01:55Z
dc.date.available2011-07-25
dc.date.available2011-07-25T17:01:55Z
dc.date.issued2011
dc.identifier.urihttps://studenttheses.uu.nl/handle/20.500.12932/7580
dc.description.abstractParkinson’s disease (PD) is a slowly progressive disease that affects approximately 6,3 million individuals worldwide. Histopathologically, PD is characterized by a progressive decreased amount of dopaminergic neurons in the brain, which ultimately leads to dopamine deficiency, deterioration of the affected brain areas and impaired brain functioning. Furthermore, Lewy bodies evolve in the damaged dopaminergic neurons, with α-synuclein as their major component. Up to now, the exact pathogenesis of PD is unknown. Although several PD-associated gene mutations have been identified, these seem to account for only a small part of all PD cases. One of the most promising indications in unraveling the pathogenesis of PD is the potential role of the α-synuclein gene (SNCA). Besides the presence of SNCA mutations, α-synuclein aggregation is found in all PD patients. Although it is still not completely clear what causes this protein to aggregate, these findings implicate there is an important role for α-synuclein in the development and progression of PD.
dc.description.sponsorshipUtrecht University
dc.format.extent1624944 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.titleAlpha-synuclein aggregation in Parkinson's disease
dc.type.contentMaster Thesis
dc.rights.accessrightsOpen Access
dc.subject.keywordsParkinson's disease
dc.subject.keywordsalpha-synuclein
dc.subject.keywordsSNCA
dc.subject.keywordsamyloidoses
dc.subject.courseuuBiology of Disease


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