Publication Date
12-2018
Date of Final Oral Examination (Defense)
11-30-2018
Type of Culminating Activity
Dissertation
Degree Title
Doctor of Philosophy in Biomolecular Sciences
Department
Biology
Supervisory Committee Chair
Brad E. Morrison, Ph.D.
Supervisory Committee Member
Allan Albig, Ph.D.
Supervisory Committee Member
Matthew L. Ferguson, Ph.D.
Supervisory Committee Member
Julia Thom Oxford, Ph.D.
Abstract
Parkinson’s Disease (PD) is an idiopathic disorder with no known cure. With number of cases steadily rising around the world, it is imperative to turn to the underlying cellular and molecular mechanisms of the disease manifestation and neurodegeneration to craft novel modes of therapy. VPS35 is one of the few genes that have identified and definitively linked to familial PD. The particular mutation that has been associated is known to cause dysfunction of a key cellular process known as autophagy. This process is primarily responsible for clearance of unwanted, damaged or misfolded proteins, among other things. Our study reveals an important link between VPS35, PI3K-AKT signaling pathway and autophagy dysfunction that might be a potential mechanism of PD pathogenesis. We also address possible perturbed dopaminergic neurogenesis in the substantia nigra brain region as a second plausible disease mechanism, as well as a target for therapeutic intervention.
DOI
10.18122/td/1488/boisestate
Recommended Citation
Rahman, Abir Ashfakur, "Investigating Autophagy Dysfunction Induced by a Parkinson's Disease-Causing Mutation in VPS35" (2018). Boise State University Theses and Dissertations. 1488.
10.18122/td/1488/boisestate
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