Scientific Writing Proposal

Morgan Roney

BIOL293- Cell Biology

TR 11:00-12:15

September 6, 2016

Scientific Writing Proposal

My name is Morgan Roney and I am a Junior here at Old Dominion University. I am majoring in Biology with a pre-veterinary focus and have thoroughly enjoyed my experiences at the university. I was drawn to major in Biology because I am very interested in the study of life and all of the various roles played by different organisms. I believe that it is interesting how each living organism has similar characteristics, but are unique at the same time. I was drawn closer to the major when I became an ambassador for the College of Sciences. As an ambassador, I get to express my interests in Biology to prospective students. The College of Sciences has also helped with ensuring that the major was the right one for my chosen career field.  Because Biology is so broad, there are many different routes available when it comes to careers and research.

In this course, I want to learn more about cells and how they contribute to the body, as well as the immune responses to various diseases. I became more interested in cells over the summer during my ten-week research internship at Virginia Tech. My research there involved Herpes Simplex Virus II Latency Associated Promoter 2 and how it contributes to neuron specificity of infection. Due to my research experience, my knowledge has expanded heavily in the study of neurons and how they work. I also have an interest in how cells contribute to different diseases and how the immune system responds to the various diseases.

My goal by the end of the course is to understand more about how cells contribute to the body as a whole, as well as the brain. I need to follow up on this because it will help in personal use and I will be more informed about how the immune system reacts to certain illnesses. Because I come from a family with various sicknesses/diseases, I have become curious about how the diseases contribute to their bodies and how exactly the sickness came about. I would like to have the ability to know more about the sicknesses in their time of need. I will relate this to course objective number two, because I am interested in seeing how cells respond to stimuli in their environments.




Final Alzheimer’s Draft

                                                                        October 30, 2016

Alzheimer’s Disease is a disease that causes brain disorder over a period and can lead to memory loss, lacking skills to think properly, and the ability to carry out simple tasks. The disease is known to be one of the leading causes of death in America, affecting more than five million people (“Alzheimer’s”). Alzheimer’s disease is formed from amyloid beta insoluble plaques that form in the brain. Amyloid beta is a short peptide that is a byproduct of amyloid precursor protein that has an unclear function. The form of the amyloid beta protein that is associated with the formation of plaques in the brain is fibrils. It is also affected by tau proteins that are expressed in neurons considering the disease to be a tauopathy (“Biochemistry”).

A monoclonal antibody is a protein made by the immune system that recognizes just one special region of just one protein. An antibody discussed was aducanumab, which was used to help reduce the amount of amyloid beta plaques found in the brain (Weintraub). Tests were run on mice to examine how the monoclonal antibody migrates to the brain. The test indicated that the antibody enters the brain and binds to amyloid beta causing the amount of plaques found to reduce (Sevigny).

The monoclonal antibody, aducanumab, is seen to selectively target the unsafe form of the plaques because it binds to the misfolded amyloid beta protein rather than the normal folded protein. Monoclonal antibodies “…target proteins that change shape and misfold, becoming toxic and triggering the hallmark beta-amyloid plaques and abnormal tau proteins…” (“Novel”). The antibody is seen to target the misfolded protein because of solubility. The antibody binds to oligomers which are soluble proteins and fibrils which are insoluble (Keller).

The data gathered in this study is used to examine how amyloid beta is affected by monoclonal antibodies in Alzheimer’s disease. The data did demonstrate, in my opinion, that the monoclonal antibody reduces amyloid beta plaques found in the brain. The antibody acts as a reducer to the plaques depending on dosage distributed. The data exhibits a change from week 26 to week 54 between the amount of amyloid plaques seen. The data concluded that the higher the dosage of aducanumab given, the lower the amount of amyloid beta plaques seen (Sevigny). This is important because this signifies the treatment is working, although it will not completely cure the disease.

The data did represent well, but not rapid enough when tested with cognitive symptoms in Child Dementia Rating (CDR) and Mini-Mental State Examination (MMSE).  The results showed that aducanumab reduced the decline in the scores of the MMSE. No improvements for the MMSE were shown between weeks 26 and 54. The results were not rapid examining that patients did not improve on the CDR when treated with placebo until week 54 of the study (Sevigny). I believe that the CDR showed better results because dose-responsiveness was seen in the tests. This means that the higher the dosage of the aducanumab, the greater the chance of positive effects to be shown.

This treatment has had a significant positive effect on the patients tested and I do believe it has promise. I believe that the FDA should cautiously approve it because I would not fully trust the treatment. The treatment should not be fully trusted because the aducanumab still produces negative effects on the patient and they could be minimized if the study is given more approach. I believe that more studies on animal models should be done before doctors start to prescribe the aducanumab once it is manufactured. This will help to avoid any errors that could come up when tested on humans. Although the drug has many negative effects, the positive effects outweigh and could be the start of something new for Alzheimer’s disease.

Works Cited

“Alzheimer’s Disease Fact Sheet | National Institute on Aging.” U.S National Library of Medicine. U.S. National Library of Medicine, n.d. Web. 15 Oct. 2016.

“Biochemistry of Alzheimer’s Disease.” Wikipedia. Wikimedia Foundation, n.d. Web. 15 Oct. 2016.

Keller, Danielle M. “Finally, a Big Win for a Monoclonal in Alzheimer’s.” Medscape. N.p., 23 Mar. 2015. Web. 16 Oct. 2016.

“Novel Monoclonal Antibodies Show Promise for Alzheimer’s Disease Treatment.” ScienceDaily. ScienceDaily, 20 July 2015. Web. 16 Oct. 2016.

Sevigny, Jeff. “The Antibody Aducanumab Reduces Aβ Plaques in Alzheimer’s Disease.” Nature. N.p., 31 Aug. 2016. Web. 15 Oct. 2016.

Weintraub, Karen. “Alzheimer’s Drug Shows Promise in Small Trial.” Scientific American. N.p., 2016. Web. 15 Oct. 2016.