The research paper deals with specific pathophysiologic pathways to better explain Parkinson’s Disease, wherein overexpressed (GPR37) protein bodies are observed in abundance. In detail, it takes into account the probability that accumulation of unfolded protein aggregates is not sole definitive cause for such degenerative status. Through a combination of laboratory techniques and embryonic kidney samples, outcomes of the study reveal that human body’s compensating mechanisms increase significant protein degeneration in motor neural functions. Additionally, several conjecture are presented, such as whether similar protective processes are adequate compensations or other controlled conditions can induce excess GPR37 protein or not.
The introduction phase of the paper deals with factual situation on Parkinson’s Disease; giving adequate medical background and moving on to expound on what the paper wants to accomplish. Focal to the study is the phenomenon of protective mechanism, specifically macroautophagy, as a process triggering neural destruction and eventual cell degeneration–a case point in Parkinson’s Disease. With the hypothesis in place, methodology seems to have answered some of the salient points in the research, such as the significant role of various treatment reagent in inducing function and clearance of inhibitory proteins (GPR37) in neural networks, as well as confirmation of seemingly direct relation between dysfunctional receptors and presence of autophagic bodies in response to the increase of the former.
In spite of such manifestations, rumination lacks impartiality; as there is selective presentation of information. Consequently, what the paper initially established has long been medically acknowledged regarding the existence of overly reacting macroautophagic encounters, wherein large numbers of defective receptors elicit automatic immunologic responses. Relative material outcome is approached in various forms, one that is comprehensively discussed below. Nevertheless, the novelty of such finding is deemed, in a way, curtailed because not all figures are in its full context. The downside is that background facts only share about actions that eventually affirm goals primarily inferred, and less management is accomplished on incriminating data–exploits that might contradict the proposals of the paper. There is bias, hence, experimental goals are assumed fraught with defensive loopholes to look after self-interests.
Management of Methods and Results
The actual investigation and interpretation of data are exhibited in an organized manner. The methods alone, from the utilization of a variety of medium (several reagents and pharmacological substances) to the analytical manipulation of the cellular samples, are executed in clear and professional mode. Even in presentation of the results, every step of the process is accounted for and logically described. Moreover, there is clarification of distinct mechanisms in eliminating excess GPR37 receptors in the system; as normal processes (proteasome functions) of disposing surplus receptors proved ineffectual, substantial influx of autophagic bodies serves solid reinforcement. Such operation is profound in Parkinson’s Disease, for early prevention can impact the lives of high risk clients. Although, the information is clearly delineated in every page, several things are still left out in the process. For one, though the goal of the paper is to prove that Parkinson’s Disease is primarily activated by the demolition of differentially increased defective GPR37 receptors, the assumption that the mounting loss also affects normal receptors are never validly proven. In a study on hepatic cells, relevant information discloses one important trait of autophagic system; there is a “degree of specificity and selectivity” during the actual disposal of cellular wastes (Yin, Ding, and Gao 1779). Such characteristic action objectively shows the important aspect of GPR37 receptors, an influential proof that defective ones are removed, while well-functioning receptors are left alone. Although this had been mentioned in the original research, the issue has fully been disregarded as insignificant to the study.
Another concern sidestepped in the methodological phase is the impact of overexpressed protein in neurologic performance. In most cases, discussion centers on manipulating samples, yet, even the experiments do not have sufficient follow through regarding the possibility of dysfunctional autophagic operations. The issue on ineffective macroautophagy is never taken up in the entire study, rendering it limited. According to Jillenger, the overproduction of autophagic bodies is not the ultimate source for excess receptor aggregates; instead, malfunctioning ones are the crux for cell death–leading the neural loss (1125). There is a conclusive evidence that such phenomena is possible, as faulty body mechanisms are more valid than high elimination rate of protein receptors–human body has compensating mechanisms to prevent such occurrences.
Relevance of Research Discussion
In the discussion stage of the research report, relevant outline has been subsequently arranged, giving important rationale in accordance with how they are presented in the result category. This section summarizes the activities performed in the method section, and at the same time, affirms the presented data. With a series of chemical manipulations, the desired responses are generated, such as when GPR37 units are significantly increased in various conditions, either with inhibited normal proteasomal systems or when status of ER stress is heightened for escalation of receptor reactions. In opposite category, constraints are placed for autophagic enactment in neural pathways, paving way for possible interventions in this area; pharmacologic obstruction has proven to be effective in suppressing macroautophagy, thereby reducing the risk of massive neural loss. In these instances, the study shows relative progress in GPR37 receptor interruption of neural damage.
Contrarily, the proposal on the direct link of cell death and degenerative cases are not reliable enough, since the exact feature of cell apoptosis (death) has not been theoretically established, hence, precise interruption is also not an option, yet (Hotchkiss, Strasser, McDunn, and Swanson). The central theme in the discussion is on implication of rapid rise in dysfunctional GPR37 receptor and their subsequent clearance, giving way for collective losses in the system. Furthermore, medical application is at preventive levels to avoid such events. Yet, topics veer on future possibilities, without presenting the limitation of the paper. Nonetheless, the discussion has been comprehensive on what matters in the paper. Beyond the margin is quite elusive, which means the paper still needs several workouts for more breadth and depth on the topic at hand.
All in all, the paper looks promising, especially on the issue on Parkinson’s Disease. The notion that there is another cause for the condition instigates massive support, yet, its incomplete presentation still needs extensive analysis. Nevertheless, the research demonstrates subjective characteristics, as it does not present the limitation of the study and lacks dual authenticity in portraying all dimensions of the research, even to the extent of refuting the set goals of the study. Yet, these are minor oversights that must be addressed to make the research for credible for critics.
Hotchkiss, Richard S., Andreas Strasser, Jonathan E. McDunn, and Paul E. Swanson. “Cell Death.” The New England Journal of Medicine 361 (2009): 1570-1583. Print.
Jillenger, Kurt A. “Recent Advances in Our Understanding of Neurodegeneration.” Movement Disorder 116 (2009): 1111-1162. Print.
Yin, Xiao-Ming, Wen-Xing Ding, and Wentao Gao. “Autophagy in the Liver.” Hepatology 47