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dc.contributor.advisorPierce-Shimomura, Jonathan T.
dc.creatorYu, Cheong Maria
dc.date.accessioned2017-08-17T15:39:09Z
dc.date.available2017-08-17T15:39:09Z
dc.date.issued2014
dc.identifierdoi:10.15781/T2PN8XX1M
dc.identifier.urihttp://hdl.handle.net/2152/61437
dc.description.abstractMany neurodegenerative diseases are characterized by abnormal accumulation of proteins, including tauopathies such as Alzheimer's disease (AD). AD is the most common form of dementia that is characterized by cognitive losses and neurodegeneration. Due to the presence of genes homologous to human genes known to be involved in AD development, the nematode Caenorhabditis elegans can be used to model neurodegenerative diseases such as AD. Here I contribute to the available nematode models by creating a new multi-copy overexpression tau model, generating the tools needed to create a single-copy overexpression tau model. I made and characterized a transgenic model expressing an extra-chromosomal array of a mutant form of tau (tau-P301L) driven by the promoter for the worm homolog of tau. Like a previous tau overexpression strain, this strain demonstrated impaired locomotion and decreased egg-laying relative to wild-type controls. However, the current model shows an adult-onset rather than larval-onset of behavioral impairments. A single-copy integration of the tau mutant for which I prepared the constructs, will help to determine if the later onset in the current model is does or location sensitive. Adult onset of impairments is an improvement over earlier onset in that it is easier to explore neurodegeneration outside of the context of development.en_US
dc.language.isoengen_US
dc.relation.ispartofHonors Thesesen_US
dc.subjectnematode modelen_US
dc.subjecttauen_US
dc.subjecttauopathyen_US
dc.subjectAlzheimer's diseaseen_US
dc.titleUtilizing C. elegans to model tauopathyen_US
dc.typeThesisen_US
dc.description.departmentNeuroscienceen_US
dc.rights.restrictionOpenen_US


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