Amyloid-beta (A4) Precursor Protein (APP)

This web page was produced as an assignment for an undergraduate course at Davidson College.

Figure 1. The amyloid-beta peptide in its two forms. The structure on the left shows the peptide when interacting with the membrane. The structure on the right shows the form in the amyloid fibril. Image taken from Protein Data Bank (2006) through the work of David Goodsell, Permission Granted.

 

Science has always been a field of great debate and discovery. However, what is the acquisition of knowledge if it is not adeqately shared. This webpage will review and compare popular press articlesObesity Today, Alzheimer's Disease Tomorrow and Midlife Obesity Linked to Alzheimer's to scientific article Amyloid Precursor Protein in Brain and Fat in the pursuit of demonstrating the significant differences in the ways in which scientific findings are relayed to the public. This analysis is in no way intended to discredit or degarde the mentioned articles; it is simply ponteing out differences between the presentation of the contextual science regarding the APP gene and its link between Alzheiner's Disease and Obesity.

 

First, we will start off with the scientific article Amyloid Precursor Protein in Brain and Fat:

In summarizing the article, the follow main points were made regarding the relationship between the Amyloid Precursor Protein (APP), obesity, and Alzheimer’s Disease (AD):

  1. Obesity during the mid-life stage posed an increase risk for AD independent of other conditions (data suggest that APP expression or function may be involved in the pathophysiology of obesity)

  2.  The study consisted of using C57BL6/J mice to create a high fat diet-induced model of obesity to determine whether the expression of APP in the brain similarly changes compared to the visceral and subcutaneous fat depots in addition to seeing if these expressions are related to the pro-inflammatory changes in tissues.

  3. The mice that were fed the fat diet (using a standard high fat feeding paradigm) demonstrated increased brain levels of APP and other pro-inflammatory proteins, compared to the control mice. Used 24 mice over a span of 22 weeks

  4. Used Western blot to see the levels of proteins of the mice

  5. Because of the correlation between the increased pro-inflammatory, neurodegenerative phenotype and the similarly increased levels of APP (and other proteins), it can be concluded that the function of APP may influence the metabolic changes that occur in each tissue during the diet-induce obesity.

 In reading the article, we are presented with hard factual data and evidence (data statistics, charts, graphs, etc.) that backs up the assumptions made; however, at times the jargon can be hard to follow or understand. Despite its difficulty to comprehend, the article provides us with a thorough examination of the assumptions, methods of data collection, results, etc. The only barrier is breaking the terminology down to suit the general public.

 

Now we will move on to the first popular press article:

Obesity Today, Alzheimer's Disease Tomorrow

Now, in keeping the scientific article in mind, let’s explore what this article has to present.  This article briefly discusses a study that has lead scientist to believe that there could be a correlation between obesity and Alzheimer's Disease in relation to the bodily levels of insulin.  The article starts off by stating, “People with diabetes are at particularly high risk of Alzheimer’s Disease”. Find this slightly problematic? Well so do I, but let us venture even further. The article goes on to state that “strong evidence” has linked having high insulin levels to potentially developing Alzheimer’s due to the proposal that insulin triggers the buildup of the beta-amyloid protein (synonymous with our APP gene) initiated by the brain inflammation caused by the increased insulin. Lastly the article concludes with a concise debriefing of the method used to attain this information (16 participants that agreed to receive 2 hour infusion of insulin and sugar, followed by a spinal tap to analyze the fluid) and how important it is to take care of our brains.


Now, let us go back to our first noted issue. The article starts off by saying that people with diabetes have an increased risk of developing Alzheimer’s. While this may be true, in the context of what was being analyzed, the inclusion of obesity was not an active factor in this matter. By scattering the idea of obesity in the article, the author is indirectly inferring that there is a correlation between diabetes and obesity, when this is not necessarily the case. There are millions of individuals with diabetes that are not obese. With this being said, the author should have given preliminary statements linking the factor of obesity with the factor of diabetes for clarity. Additionally the article makes references to “strong evidence” and fails to provide some sort of factual, concrete apparatus to convince us of these conclusions. No good lay reader should just accept what is being read without adequate information to support claims.

 

Last but not least, our second popular press article:

Midlife Obesity Linked to Alzheimer's 


This last article is based off of the research efforts of the Framingham Heart Study, which reaffirms the concluded link between mid-life obesity and Alzheimer’s, in addition to presenting other contributing factors, such as high blood pressure, diabetes, and smoking. The article briefly discusses the decrease of brain volume in relation to the aforementioned factors, providing examples of these effects, such as the link between obese individuals having a decline in test scores and experiencing difficulty in various tasks such as abstract thinking.  In mentioning various research projects, if the reader was truly interested, he or she could look up the various efforts to learn more. On the other hand, the article was vague as to providing details of how measures were carried out, facts about the research. Additionally Alzheimer’s was only mentioned once (not including the title), which seemed a little counterproductive.

 

Conclusion:

As shown in Figure 2. there are a number of differences that distinguish scientific article from popular press articles. Some of these differences can be for better or for worse or both. As shown in the case of “Midlife Obesity” article, appealing to the emotions could be a pro or a con. While appealing to emotions would rally the masses to start being concerned with health issue and the genetics behind it, if the wrong information is presented or presented in a way which is skewed or misleading then appealing to the people would only cause further confusion of science and mislead efforts. Above all, the major take home is that despite these differences, each type of article has its place in reporting news, research, etc. Although there is a general difference between scientific and popular press articles, the level of the popular press article greatly vary which brings back the importance of choosing your sources wisely and appropriately for its intended use.

 

  APP in Brian and Fat (Scientifc) Obesity Today, Alzheimer's Tomorrow (Popular Press) Midlife Obesity Linked to Alzheimer's (Popular Press)
Pros
  • Includes figures and data to show the reader the specifics of what is going on
  • Very in depth
  • Concise, a quick read
  • Includes a brief overview of the methods without overwhelming the reader with details
  • Uses everyday jargon which is easier for the reader to understand
  • Concise, a quick read
  • Uses everyday jargon which is easier for the reader to understand
  • Appeals to emotions
Cons
  • Hard to understand
  • Takes more time to read and analyze
  • Can have misleading statements
  • Make statements without including further supporting data
  • Very vague as to what resesearch is being used
  • Appeals to emotions
  • No hard facts or details included
  • A little scattered in terms of focus
Figure 2. The chart depicts a comparison of the pros and cons of the scientific article and the two other popular press articles. The figure was self-produced.

 

References:

DeNoon, D. (2005). Obesity and alzheimers. Obesity Today, Alzheimer's Disease Tomorrow?, Retrieved from http://www.webmd.com/alzheimers/guide/20061101/obesity-alzheimers-risk

Goodsell, D. (Producer). (2006). Exploring the structure. [Web Graphic]. Retrieved from http://www.pdb.org/pdb/101/motm.do?momID=79

LiveScience. (2011). Midlife obesity linked to alzheimer's. Mother Nature Network, Retrieved from http://www.mnn.com/health/fitness-well-being/stories/midlife-obesity-linked-to-alzheimers

Puig, K., Floden, A., Adhikari, R., Golovko, M., & Combs, C. (2012). Amyloid precursor protein and proinflammatory changes are regulated in brain and adipose tissue in a murine model of high fat diet-induced obesity. PLos ONE, 7(1), Retrieved from http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030378

 

 

 

 

 


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