Barrett, The Honors College Thesis/Creative Project Collection
Barrett, The Honors College at Arizona State University proudly showcases the work of undergraduate honors students by sharing this collection exclusively with the ASU community.
Barrett accepts high performing, academically engaged undergraduate students and works with them in collaboration with all of the other academic units at Arizona State University. All Barrett students complete a thesis or creative project which is an opportunity to explore an intellectual interest and produce an original piece of scholarly research. The thesis or creative project is supervised and defended in front of a faculty committee. Students are able to engage with professors who are nationally recognized in their fields and committed to working with honors students. Completing a Barrett thesis or creative project is an opportunity for undergraduate honors students to contribute to the ASU academic community in a meaningful way.
Parkinson’s disease (PD) is a debilitating neurodegenerative disease characterized primarily by physical impairments such as tremors, poor balance, and bradykinesia; however, some individuals with PD will additionally experience numerous nonmotor symptoms such as dementia, depression, and sleep disturbances amongst various other life-altering ailments. Two of the key pathological hallmarks of…
Parkinson’s disease (PD) is a debilitating neurodegenerative disease characterized primarily by physical impairments such as tremors, poor balance, and bradykinesia; however, some individuals with PD will additionally experience numerous nonmotor symptoms such as dementia, depression, and sleep disturbances amongst various other life-altering ailments. Two of the key pathological hallmarks of PD include the death of melanated dopaminergic neurons in the nigrostriatal pathway and the accumulation of Lewy bodies, which are primarily composed of aggregates of the protein α-synuclein (α-syn). Interestingly, members of the chitinase protein family, namely chitinase-3-like protein-1 (L1), have heightened concentrations in a number of neurodegenerative diseases other than PD. To investigate the specific role L1 plays in PD etiology, we evaluated if astrocytic L1 expression was elevated in postmortem brain tissue of PD patients as well as in an α-syn overexpression rat model, and further tested if manipulating astrocytic-specific L1 expression correlated with neuroinflammation and nigral neuronal degeneration in the model. Preliminary histological analysis has shown increased levels of L1 expression in the α-syn model before neuronal loss occurs, and in human tissue, L1 was found to be significantly increased in the postmortem tissue of individuals with PD versus non-diseased controls. Investigations in identifying an astrocytic-specific virus capsid and manipulating L1 expression in the α-syn model are ongoing. This preliminary data thus far supports that increased astrocytic expression of L1 is associated with PD pathology.
