Preprint / Version 1

Metal Intake & Exposure Manipulation on Prion Aggregation and Disease Pathogenesis: Analysis & Experimental Paradigm

##article.authors##

  • Atul Kashyap Centennial Highschool

DOI:

https://doi.org/10.58445/rars.932

Keywords:

Prion, Neurodegeneration, Neuroscience, Proteins, Biochemistry, Public Health, Medicine

Abstract

There has long been ambiguity regarding the biomolecular solutions for mitigating prion aggregation and development in vivo, much of which has stagnated in early experimental phases. To understand the main function of metallic cofactors in the development of neurodegenerative diseases, researchers have been conducting preclinical trials on mice, and have found that metal intake coupled with high oxidative stress positively correlates with increased rates of prion related neurodegeneration. The purpose of this study is to outline the general pathogenesis of prion diseases, and propose possible epidemiological and biomolecular guidelines to limit prion aggregation and prevalence rates. This study was primarily conducted through a series of literature reviews in order to consolidate the hypothesis that changes in metal exposure can indeed change the rates of prion disease pathogenesis. The results of the literature reviews generally supported the claim that reducing/increasing metal intake to evolutionarily required concentrations and limiting aqueous metal ion exposure will aid in the reduction of disease development and prion aggregation, which allowed the researcher to come to the conclusion that manipulating the influx and exposure to metal is an epidemiologically viable option for reducing the rampant rates of prion related death, ultimately reducing clinical and financial stress on the global healthcare setting. The aforementioned literature review was then used to design and outline a possible experimental paradigm to test the manipulation of metal levels in mouse brain homogenate in vivo.

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Posted

2024-02-03