My name is Grace Porter, and I am a recent graduate of the University of Georgia with Bachelor of Science degrees in both Biology and Genetics. As an undergraduate, I participated in research under Dr. Shiyou Chen of the Department of Physiology and Pharmacology to examine the effects of a gene known as DOCK2 on development of atherosclerosis and hypertension in mice. During my tenure as a SENS Research Foundation Summer Scholar, I was given the privilege to work in Dr. Julie Andersen’s lab at the Buck Institute for Research on Aging; for ten weeks I worked to investigate interrelated hallmarks of Parkinson’s disease (PD) under the guidance of post-doctoral fellow, Dr. Georgia Woods. Relevant to both the SENS Research Foundation’s and the Buck Institute’s missions to support research on aging as a mechanism of disease, the Andersen lab works to further our understanding of the underlying mechanisms of neurodegenerative diseases such as Parkinson’s disease. Specifically, the Andersen lab examines the effects of various cellular stressors, such as inflammation, and their related impact on PD progression.
Over the course of my time in the Andersen lab, I examined a specific Parkinson’s disease mouse model that readily displays the aggregations (clumping) of mis-folded alpha-synuclein protein commonly found in PD patients in formations known as Lewy Bodies. The disease model is official known as the pre-formed fibril (PFF) induced alpha-synuclein aggregation mouse model. When observing this model, I worked to investigate the linkage between brain inflammation and protein aggregation in Parkinson’s disease and its progression. My research examined the possibility of a protein known as High- mobility group box 1 (HMGB1) as a possible inflammatory molecule released in response to protein aggregation and other cell stressors. The study of HMGB1 can assist in finding connections between the interrelated hallmarks of Parkinson’s disease: neuroinflammation, protein aggregation, and irreversible loss of dopaminergic neurons that ultimately leads to impairment of motor function. By the time patients afflicted with PD display the physical symptoms, over 60% of their dopaminergic neurons are lost and unable to be recovered or repaired. Importantly, HMGB1, if found to display an interactive role in Parkinson’s progression could serve as a viable drug target to slow or halt PD progression or, at the very least, serve as an indicator of disease before irreversible loss of dopaminergic neurons.