This web page was produced as an assignment for Genetics 677, an undergraduate course at UW-Madison.
A Comparison of Popular Press and Scientific Articles
Note: To read a summary of the popular press article "Communication breakdown: What happens to nerve cells in Parkinson's disease", click here. For a summary and pdf link to the scientific article "SH3 Domains from a Subset of BAR Proteins Define a UbI-Binding Domain and Implicate Parkin in Synaptic Ubiquitination", click here.
Both the popular press (Science Daily) and scientific (Molecular Cell) articles I reviewed described the same study done by researchers at McGill University. The popular press article fared well in explaining the major finding of the study, namely parkin's interaction with endophilin-A. The scientific article managed to detail the interactions between the two proteins, yet this was done in more technical terms. The significance of the researchers' findings were clearly stated in the article by Science Daily; there would be potential treatment targets for Parkinson's Disease. The scientific article, however, deemed the implications of the results more relevant at the microscopic level, in terms of elucidating the molecular mechanisms of recessive PD.
Despite my difficulty in grasping the biological roles of the protein domains discussed in the scientific article, I was still able to understand the concepts associated with their binding affinites. For example, the authors use protein binding assays in their figures for a side-by-side comparison of wild type and knock out mutants of in showing binding ability with endophilin-A. Such figures were able to convince me of a particular domain’s importance in binding without having any knowledge of its mechanistic features. Like many well written science papers, the thought processes of the experiments were detailed alongside with the results and in a logical order.
The Science Daily article supplied enough background information to convey the link between the parkin mutation and the neurological degeneration found in PD. I found the article’s description of the methods used in the study to be broad stroke and inadequate for the curious reader. However, the article gave enough detail on the experiment as to direct focus onto the interaction between parkin and endophilin-A. One of the biggest strengths of the article was defining the implications of this research, which was finding new treatment targets for PD.Many times, reporters that are eager to engage an audience will implicate research findings to areas beyond the scope of the study. This was not the case for the article by Science Daily. I was impressed by the integrity of reporting done on characterizing what has been found about parkin’s role in PD. For example, the author uses the preface that “the function of the parkin protein is not yet well defined” before describing the putative mechanisms of the protein’s functions. Additionally, the article presents well-rounded insight into the research findings from members of the scientific community, including the CIHR director, a post doc, as well as the principal investigator himself.
In terms of factual content, the scientific paper clearly had more. Whether or not the additional information found in the science paper is beneficial depends upon the reader's background. The consistent use of structural protein jargon in Molecular Cell's paper could confuse readers with a basic biology background, let alone an armchair scientist. Nonetheless, reading through the results and figures of the scientific paper proves to be a rewarding experience, as one is able to see the steps that recessive PD takes in becoming pathogenic. Thus, the popular press article lacks the molecular specificity when discussing the study but makes up for it in brevity. Hence, someone with little knowledge on parkin or PD is best suited to read the Science Daily article whereas those with a solid understanding of molecular biology would enjoy the paper in Molecular Cell.
Both the popular press (Science Daily) and scientific (Molecular Cell) articles I reviewed described the same study done by researchers at McGill University. The popular press article fared well in explaining the major finding of the study, namely parkin's interaction with endophilin-A. The scientific article managed to detail the interactions between the two proteins, yet this was done in more technical terms. The significance of the researchers' findings were clearly stated in the article by Science Daily; there would be potential treatment targets for Parkinson's Disease. The scientific article, however, deemed the implications of the results more relevant at the microscopic level, in terms of elucidating the molecular mechanisms of recessive PD.
Despite my difficulty in grasping the biological roles of the protein domains discussed in the scientific article, I was still able to understand the concepts associated with their binding affinites. For example, the authors use protein binding assays in their figures for a side-by-side comparison of wild type and knock out mutants of in showing binding ability with endophilin-A. Such figures were able to convince me of a particular domain’s importance in binding without having any knowledge of its mechanistic features. Like many well written science papers, the thought processes of the experiments were detailed alongside with the results and in a logical order.
The Science Daily article supplied enough background information to convey the link between the parkin mutation and the neurological degeneration found in PD. I found the article’s description of the methods used in the study to be broad stroke and inadequate for the curious reader. However, the article gave enough detail on the experiment as to direct focus onto the interaction between parkin and endophilin-A. One of the biggest strengths of the article was defining the implications of this research, which was finding new treatment targets for PD.Many times, reporters that are eager to engage an audience will implicate research findings to areas beyond the scope of the study. This was not the case for the article by Science Daily. I was impressed by the integrity of reporting done on characterizing what has been found about parkin’s role in PD. For example, the author uses the preface that “the function of the parkin protein is not yet well defined” before describing the putative mechanisms of the protein’s functions. Additionally, the article presents well-rounded insight into the research findings from members of the scientific community, including the CIHR director, a post doc, as well as the principal investigator himself.
In terms of factual content, the scientific paper clearly had more. Whether or not the additional information found in the science paper is beneficial depends upon the reader's background. The consistent use of structural protein jargon in Molecular Cell's paper could confuse readers with a basic biology background, let alone an armchair scientist. Nonetheless, reading through the results and figures of the scientific paper proves to be a rewarding experience, as one is able to see the steps that recessive PD takes in becoming pathogenic. Thus, the popular press article lacks the molecular specificity when discussing the study but makes up for it in brevity. Hence, someone with little knowledge on parkin or PD is best suited to read the Science Daily article whereas those with a solid understanding of molecular biology would enjoy the paper in Molecular Cell.
References
1. McGill University (2010, February 10). Communication breakdown: What happens to nerve cells in Parkinson's disease. ScienceDaily. Retrieved February 22, 2010, from http://http://www.sciencedaily.com/releases/2010/02/100209200803.htm
2. Trempe, J., Chen, C., Grenier, K., Camacho, E., Kozlov, G., McPherson, P., Gehring, K., and Fon, E. (2009). SH3 Domains from a Subset of BAR Proteins Define a UbI-Binding Domain and Implicate Parkin in Synaptic Ubiquitination. Mol Cell, 36 (6), 1034-47.
2. Trempe, J., Chen, C., Grenier, K., Camacho, E., Kozlov, G., McPherson, P., Gehring, K., and Fon, E. (2009). SH3 Domains from a Subset of BAR Proteins Define a UbI-Binding Domain and Implicate Parkin in Synaptic Ubiquitination. Mol Cell, 36 (6), 1034-47.
