Date Thesis Awarded

5-2024

Access Type

Honors Thesis -- Open Access

Degree Name

Bachelors of Science (BS)

Department

Neuroscience

Advisor

Randolph Coleman

Committee Members

Christy Porter

Lisa Landino

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disease across the world, affecting over 6 million people worldwide. This disorder is characterized by the progressive loss of dopaminergic neurons within the substantia nigra pars compacta (SNpc) due to the aggregation of α-synuclein within the brain. Patients with PD develop motor symptoms such as tremors, bradykinesia, and postural instability, as well as a host of non-motor symptoms such as behavioral changes, sleep difficulties, and fatigue. The reduction of dopamine within the brain is the primary cause of these symptoms. The main form of treatment for PD is levodopa, a precursor to dopamine that can cross the blood-brain barrier (BBB). Levodopa reduces PD symptoms by increasing dopamine levels. While L-Dopa is often used as the primary pharmaceutical for PD, it comes with many drawbacks with long-term use. 40% of patients develop complications with levodopa within five years of treatment. A new emerging Parkinson’s treatment is ketamine, which has been shown to produce long-lasting benefits for PD patients. Ketamine reduces motor complications and produces neuroprotective effects within the brain. Using current neuroscience literature, a mathematical model created in CellDesigner depicts the neurological pathways of these medications within the brain. Using a biochemical system simulator, COPASI, these models investigate the effects of levodopa and ketamine on a diseased brain system. Model results aligned with current literature and highlighted key areas for future research.

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