Thesis (Ph. D.)--Michigan State University. Dept. of Neuroscience, 2008. / Title from PDF t.p. (viewed Sept. 11, 2009). Includes bibliographical references (p. 271-303). Also issued in print.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 1993. / Vita. Abstract. Includes bibliographical references (leaves 209-226). Also available via the Internet.

Thesis (P.hD)) - University of Queensland, 2004. / Includes bibliography.

Thesis (Ph. D.)--University of Wisconsin, 1964. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Bibliography: leaves 249-258.

Thesis (M.A.) University of Missouri-Columbia, 2004. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file viewed on (June 30, 2006) Vita. Includes bibliographical references.

Thesis (B.Sc)--University of Hong Kong, 2001. / "A dissertation submitted in partial fulfilment of the requirements for the Bachelor of Science (Speech and Hearing Sciences), The University of Hong Kong, May 4, 2001." Also available in print.

Thesis (M.M.) Florida State University, 2007. / Advisor: Jayne Standley, Florida State University, College of Music. Title and description from dissertation home page (viewed 8-29-2007). Document formatted into pages; contains 65 pages. Includes biographical sketch. Includes bibliographical references.

Thesis (M.Sc.)--University of Melbourne, School of Physiotherapy, 2009. / Typescript. Includes bibliographical references (leaves 107-116)

No description available.

α-Synuclein (αSyn) is a small intrinsically disordered protein that drives the progression of a group of neurological disorders known of synucleinopathies, including Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Increased expression of αSyn due to gene duplication or triplication causes familial forms of these diseases, of which the severity is positively correlated with the gene copy number. Despite extensive efforts using various models, the precise mechanisms of αSyn toxicity in neurons have not been elucidated. This could be partly due to biological differences between the models and authentic human neurons. In an attempt to model synucleinopathies with human neurons, I have established a collection of transgenic human embryonic stem cell (hESC) lines over-expressing αSyn. I first showed that elevated αSyn expression does not affect hESC proliferation and their differentiation potential towards neurons. Then I identified transgenic hESC lines that maintained high αSyn expression in differentiated neurons and compared the rate of reactive oxygen species (ROS) production in high versus normal αSyn expressing cortical neuronal cultures. I observed a significantly elevated level of ROS production in αSyn over-expressing neurons in less mature neurons; however, there was no difference observed in more mature neurons. The possible reasons that lead to this difference are discussed. This is the first report of stable αSyn overexpressing hESC lines, which can provide an unlimited source of human neurons for studying the mechanism underlying neuronal cell death in synucleinopathies, which in turn could lead to the development of potential therapeutics.