Kalil-Roldán, J., Román-Vega, R., Rivera-Crespo, Y., Colón, J., Alves, J., Inyushin, M.

Department of Physiology, Universidad Central del Caribe, Bayamon, PR

Department of Microbiology & Immunology, Universidad Central del Caribe, Bayamon, PR


Amyloid beta accumulation is associated to the neurocognitive decline of patients with Parkinson’s Disease as well the collectively classified HIV-Associated Neurocognitive Disorders. Neuroinflammation brought on by these diseases promotes the aggregation and degranulation of platelets. Platelets in turn release amyloid beta precursor protein which is subsequently cleaved in platelet-associated micro vessels as well as by endothelial cell enzymes to form amyloid beta.

Production of amyloid beta exacerbates the proinflammatory response by affected cells, thereby forming a positive feedback loop with its deposition in blood vessels. Thus, we hypothesized that both Parkinson’s Disease pathologies and Gp120 HIV protein, which have been shown to elicit this proinflammatory response in the brain, could explain not only the development of dementia in patients with Parkinson’s and the development of HIV Associated Neurocognitive disorders but also the accumulation of amyloid beta. Gp120 elicits inflammation by promoting the secretion of cytokines. Furthermore, 6-Hydroxydopamine is injected in rat brains to promote dopaminergic cell death in the substantia nigra (which is the hallmark characteristic of PD pathology). The objective of the present study was to establish the presence of amyloid beta protein in tissues and blood vessels undergoing degeneration mediated by injected 6-OHDA neurotoxin and Gp120.

Immunohistochemical staining confirmed the presence of AB in blood vessels adjacent to tissues undergoing cell degeneration. In addition, ELISA Assay show increased concentrations of AB 1-40 peptide in tissues treated with either Gp120 or 6-OHDA when compared to negative control tissues. The identification of amyloid beta deposits in blood vessels and tissues of 6- Hydroxydopamine and GP120 injected rats is a step forward in understanding the processes involved in the inevitable transition of Parkinson’s to dementia as well the development of HIV Associated Neurocognitive disorders.

Acknowledgments:

Supported by Universidad Central Del Caribe (UCC), The Alliance-NIMHD-NIH, Expanding

Undergraduate Students Education, Opportunities and Options in Clinical and Translational

Research Supported by the US Department of Education: Title V Grant Award#P031S160068 and

MAC-FRED Program 2018.

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