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.
“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.