Pathophysiology of Parkinson's Disease - Essay Sample

Introduction

Pathophysiology is a medical term that refers to the anarchic physiological processes linked with a syndrome or injury (Jankovic, 2016). Parkinson's disease is a significant element in the Pathophysiology family. With the genes involved, the patterns of inheritance will always differ accordingly, according to the reported cases of Parkinson's. Parkinson's is an age-related disease, which is neurodegenerative, and some of the characteristics of this disease are Lewy pathology, dopaminergic neurons, and midbrain loss. A genetic mutation of the genes has been the result of the family linked cases for the disease, whereby a good portion of the disease conduct can be traced back to family history. These genetic mutations have been found in genes, including; PINK1, PARK2, SNCA, LRRK2, or the PARK7 gene (Pereira et al. 2016). All these genes have been linked directly or indirectly to Parkinson's disease, and hence, this paper seeks to understand the interaction between genetic changes and the individual risk of contracting the diseases.

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Author’s Research Focus

Although a general understanding of the risk of developing the disease to an individual has not been unveiled, the interaction between genetic changes, or mutations, and an individual’s remains, the alpha-synuclein protein's making occurs in SNCA. The Lewy bodies are the protein clumps that gather in the individuals' brain cells for Parkinson’s disease carriers. During the initial stages of the occurrence of the disease is when the Mutations of the SNCA are witnessed. For the PARK2, the recycle of the proteins and the cells' breakdown occurs, making the protein parking (Cataldi et al. 2018). The mitochondrial stress is protected by the PARK7 gene, which is made by the protein DJ-1. Also, the early signs are witnessed in the mutations in this gene cause. The PINK1 mutations are also witnessed in the disease's initial phases, the Parkinson’s', where the protein kinase with continued protection on the mitochondria structures from stress. Again, the protein kinases are made in the LRRK2. The late stages of Parkinson’s disease are characteristic of the Mutations (Cataldi et al. 2018).

The substantia nigra part of the brain, which deals with controlling body movement and balance, is the major focus of Parkinson's disease. Further, the researcher indicates that the disease affects the nervous system and is progressive. VP35, i.e., the vacuolar protein sorting 35, has been linked to substitution aspartate from asparagines, a late stage of the inherited Parkinson disease. This study sampled some 61 families that were unrelated and had some idiopathic clinical syndrome indistinguishable. The different clinical symptoms exhibited were the VPS29, VPS26, and the VPS35, which forms part of the retromer trimer as structural components. The retromer trimer recycles transmembrane and is complex with a pair of sorting nexin, which helps in the cell transport surface or trans-Golgi network (Pereira et al. 2016).

Research Impact

The researchers developed the retromer complex stoichiometry with a mouse model to preserve the physiological nature of the VPS35, i.e., the vacuolar protein sorting 35 (Cataldi et al. 2018). The vacuolar protein sorting 35 knock-in mice had been reported with no reference to a phenotype, which is behavioral; reduced striatal dopamine was revealed in homozygous animals with striatal micro dialysis revealed. The idiopathic has a dopamine neuron loss and is selectively vulnerable. The researchers carried out a hypothesis of Vps35 p.D620N, which was impaired and recycled with specific cargo retromer-dependent, which had consequent effects on dopaminergic neurotransmission (Wu et al. 2017). The integrity of dopamine release and the nigrostriatal system characterization was focused at three months of motor behavior. The results of the study areas are indicated in the subsequent section.

Personal Discovery

The study aimed at examining the effects of the VPS35, i.e., the vacuolar protein sorting, p.D620N metamorphosis at physiological stages, and keep away from overexpression and the confounds of random insertion. The littermates, mice experiment after the three months, exhibited no specific differences in appearance. Again, the researchers carried out the bruising of dopamine synthesis with the TH (tyrosine hydroxylase) and the nigrostriatal system's integrity and substantia nigra pars compacta. The study revealed no differences were significantly observed between. The dissection of the VKI mice and the Striata, metabolites, and the HPLC for dopamine tissue was homogenized, and the supernatant was assayed. The research indicated no differences in genotype in the total production of dopamine, suggesting that its metabolites in VKI mice are unaffected.

Conclusion

The research has suggested that a gross motor disfunction (memory loss) in mice at three months of age is not easily noticeable. It appears to be normal in appearance, body weight, and survival tactics. In the dorsolateral striatum, the dopamine release is not evoked, and that, there is an increased capacity of the VK1 slices. The research also identified that the idiopathic has a dopamine neuron loss and is selectively vulnerable. The genes in the dorsolateral striatum protect against the mitochondrial stress in the memory of the individual.

References

Cataldi, S., Follett, J., Fox, J., Tatarnikov, I., Kadgien, C., Gustavsson, E., & Farrer, M. (2018, August 21). Altered dopamine release and monoamine transporters in Vps35 p.D620N knock-in mice. Retrieved September 28, 2020, from https://www.ncbi.nlm.nih.gov/pubmed/30155515

Jankovic, J. (2016). Dopamine depleters in the treatment of hyperkinetic movement disorders. Expert opinion on pharmacotherapy, 17(18), 2461-2470. https://www.ncbi.nlm.nih.gov/pubmed/27819145

Pereira, D. B., Schmitz, Y., Mészáros, J., Merchant, P., Hu, G., Li, S., & Sonders, M. S. (2016). Fluorescent false neurotransmitter reveals functionally silent dopamine vesicle clusters in the striatum. Nature Neuroscience, 19(4), 578-586. doi/abs/10.1113/jphysiol.2010.200477

Wu, S., Fagan, R. R., Uttamapinant, C., Lifshitz, L. M., Fogarty, K. E., Ting, A. Y., & Melikian, H. E. (2017). The dopamine transporter recycles via a retromer-dependent postendocytic mechanism: tracking studies using a novel fluorophore-coupling approach. Journal of Neuroscience, 37(39), 9438-9452.