Article Critique: Interaction Between Neuromelanin and Alpha-Synuclein in Parkinsons Disease

This article seeks to look into the interaction between Alpha-Synuclein (a-syn) and Neuromelanin (NM). The main research problem being addressed in this article is the Parkinsons disease (PD), a common disorder that is neurodegenerative and characterized by a-syn accumulation into Lewy body inclusions and the loss of NM containing dopamine neurons in the substantia nigra (Xu & Chan, 2015).

It is clear from the articles abstract that NM and a-syn are two prominent stamps in the Parkinsons disease. The authors state that through various mechanisms like inhibiting protein degradation systems and inducing oxidative stress, dopaminergic neuron death can be induced by pathological a-syn. Xu and Chan (2015) start by giving the pathological features and aetiology of PD which serves to create a better understanding of the research topic. This section sets the stage for further discussions regarding PD development by providing the necessary background knowledge.

Another key issue that arises from the article is the link between Parkinson's disease and a-syn whereby the authors state that six a-syn gene missense mutations have been associated with the pathogens of PD. The authors acknowledge the toxicity nature of a-syn while supporting this hypothesis by citing the increased levels of a-syn protofibrils in PD patients brains. To shed more light on the research topic, the authors highlight the relationship between neuromelanin and Parkinsons disease. To achieve this, the authors look at the link under three categories namely neuromelanin structure and biosynthesis, NM involved in the PDs pathogenesis as well as the interaction of NM with organic and inorganic molecules (Xu & Chan, 2015). The authors provide a good description of NM before showing how it links to PD.

Having provided enough information regarding, NM and a-syn, the authors then proceed to show how the two interact. According to the authors, one of the key interaction is where NM accumulation results in an increase in the level of a-syn in SN Neurons. Also, a-syn is said to induce the NM biosynthesis. The authors conclude by agreeing on the pivotal role played by a-syn in the PD pathogenesis. The aggregates of a-syn redistribute to NM in the substantia nigra early in Parkinsons disease while NM biosynthesis is induced by a-syn through increased cytosolic levels (Xu & Chan, 2015).

Overall, this article succeeds in clearly demonstrating the interaction between NM and a-syn in Parkinsons disease through clear descriptions and explanations, reinforced with the findings of various relevant studies. As such, the article appropriately conveys information to the reader through the vivid descriptions which shed more light on the topic. Generally, the article is well-written and is able to pass the intended important message regarding Parkinsons disease.

Reference

Xu, S., & Chan, P. (2015). Interaction between Neuromelanin and Alpha-Synuclein in Parkinsons Disease. Biomolecules, 5(2), 1122-1142. doi:10.3390/biom5021122