Show simple item record

dc.contributor.authorNguyen, Andrew Huyen_US
dc.date.accessioned2015-08-04T15:57:09Z
dc.date.available2015-08-04T15:57:09Z
dc.date.issued2013
dc.date.submitted2013
dc.identifier.other
dc.identifier.urihttps://hdl.handle.net/2144/12171
dc.descriptionThesis (M.A.)--Boston Universityen_US
dc.description.abstractMutations in alpha-synuclein and leucine-rich repeat kinase 2 (LRRK2) have been implicated in the cause of Parkinson’s disease (PD). These two proteins have been the targets of a great deal of recent research that has transformed our understanding of this disorder. Recent research using C. elegans as a model species has shown that alpha- synuclein expression and the LRRK2-G2019S mutation potentiate neurodegeneration similar to that seen in cases PD. Further exploration revealed that defects in autophagy of dopaminergic neurons may be the cause for the observed pathology. In the current study, the confirmation of autophagy as a possible cause of pathology due to the expression of alpha-synuclein and the LRRK2-G2019S mutation is completed through the use of electron microscopy. We observed that large vacuoles had formed in the cephalic dopaminergic neurons of alpha-synuclein + LRRK2 transgenic samples not seen in wild-type samples. Further, large morphological changes in the nerve ring area of the transgenic nematodes were also observed that may implicate that alpha- synuclein expression in conjunction with the LRRK2-G2019S mutation may have a widespread effect on many neurons that was not previously expected.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.titleElectron microscopy analysis of alpha-synuclein and LRRK2 transgenic C. elegansen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Artsen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


This item appears in the following Collection(s)

Show simple item record