Although Parkinson’s Disease (PD) is the second most prevalent neurodegenerative disease in the U.S., the pathology remains an enigma. Many neuroinflammation hypotheses have been studied to explain its development. It’s shown that inflammatory markers such as COX-2 activity, which synthesizes the potent vasodilator PGE2, are overexpressed in PD. Additionally, astrocytes, regulators of inflammation in the brain and BBB, undergo important changes during PD. However, the vascular consequences that all this has for PD-led neurodegeneration are relatively unexplored. We conducted a systemic review of 793 articles of experimental studies that are publicly available across four online databases (PubMed, Florida International University Database, World of Science, and Scopus) related to the topic of vascularity and blood-brain barrier (BBB) in PD to summarize widely evidenced vascular changes in the disease. Present literature on astrocyte reactivity and COX-2 expression in PD was reviewed, to draw a parallel between these and the findings from our systemic analysis. Five important vascular changes were found in the systemic analysis drawn from the final 25 sources selected, with the most frequent change being an increase in BBB permeability. This observation was evidenced primarily in animal studies and was the only change noted through an in-vivo study. Other vascular changes found were a decrease in tight-junction proteins in the endothelium, the presence of angiogenesis markers, a change in vessel density, and a change in vessel width or thickness. Our literature review pointed to a connection between the function of astrocytes and the hyperactivity of COX-2 while our analysis observed changes in vascularity. The increase in BBB permeability and eventual disruption is an important hallmark of the vascular repercussions of PD. Due to astrocytes’ function in supporting the BBB and the vasodilating effect of COX-2 overexpression, we might consider this relationship a starting point for understanding neurodegeneration.
