Week 5: Background

Good to see you again! 

This week, I was writing the introduction section for my research paper. 

Here is a snippet: 

It is a well-established fact that Parkinson’s Disease is one of the most prevalent neurodegenerative conditions, affecting approximately 3% of individuals above the age of 60 years on an annual basis. Parkinson’s Disease, also known as PD, is a complex disorder that affects multiple systems and is characterized by movement abnormalities resulting from the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) (Hayes et al., 2019).  

As a result, Levodopa has been utilized as a treatment for the symptoms of Parkinson’s Disease, however, its prolonged use can lead to the development of adverse effects, including dyskinesia, dystonia, and speech impairment (Blanchet et al., 1996, p. 1). To address this issue, scientists have developed alternative therapies, specifically dopamine agonists, such as monoamine oxidase-B (MAO-B) inhibitors and Catechol-O-methyl transferase (COMT) inhibitors to alleviate the symptoms of Parkinson’s Disease whilst reducing the negative side effects associated with long-term Levodopa therapy. The utilization of COMT inhibitors as a therapeutic approach is commercialized in two forms, including Entacapone and Tolcapone. COMT inhibitors bind to the COMT enzyme and, are used in correspondence with Levodopa to block the COMT enzyme from breaking down dopamine(Yassin et al., 1998). On the other hand, MAO-B inhibitors are available as Selegiline and Rasagiline (Olanow et al., 2006). Similarly, MAO-B inhibitors are also utilized to inhibit the monoamine oxidase-B enzyme from degrading the dopaminergic neurons (Najib et al., 2001). 

Despite the availability of several countermeasures aimed at preventing the onset of PD, a viable alternative for inhibiting the formation of PD through the blocking of voltage-gated potassium channels has not yet been developed. Numerous environmental factors, including 4-Aminopyrodine, may lead to the closure of these channels, for which a cure has yet to be discovered. The primary objective of this research paper is to underscore the significance of the various ways in which PD may arise, and the creation of a motor disorder model serves as an exemplary approach to achieving this goal. The study aims to inform researchers of the need to explore diverse methods that could potentially contribute to addressing the challenges associated with PD. 

1. Blanchet, P.J., Grondin, R., Bédard, P.J., Shiosaki, K., Britton, D.R., 1996. Dopamine D1 receptor desensitization profile in MPTP-lesioned primates. Eur J Pharmacol 309, 13–20. https://doi.org/10.1016/0014-2999(96)00309-3 
2. Yassin, M.S., Cheng, H., Ekblom, J., Oreland, L., 1998. Inhibitors of catecholamine metabolizing enzymes cause changes in S-adenosylmethionine and S-adenosylhomocysteine in the rat brain. Neurochem Int 32, 53–59. https://doi.org/10.1016/s0197-0186(97)00047-8 
3. Olanow, C.W. (2006). Rationale for considering that propargylamines might be neuroprotective in Parkinson’s disease. Neurology 66, S69-79. https://doi.org/10.1212/wnl.66.10_suppl_4.s69 
4. Najib, J., 2001. Entacapone: a catechol-O-methyltransferase inhibitor for the adjunctive treatment of Parkinson’s disease. Clin Ther 23, 802–832; discussion 771. https://doi.org/10.1016/s0149-2918(01)80071-0 

Next Week: I will be traveling back to the University of Chicago to conduct my experiment and will be posting pictures of the results. See you then!