Author: Branden Chen
Editors: Shannon Tan and Katelyn Ma
Artist: Denise Suarez
Neurological disorders affect hundreds of millions of people worldwide, and one prominent example is Alzheimer’s disease. Alzheimer’s is classified as a progressive disorder that causes neurons in the brain to die and degenerate, and it is the leading cause of dementia. Dementia is the continuous decline in thinking, social, and behavioral skills that negatively affects a person’s ability to live their life independently. With Alzheimer’s disease becoming more prevalent each year, it is important to understand the research done on the causes and treatment of Alzheimer’s disease.
Although scientists have uncovered a vast amount of information regarding Alzheimer’s disease, the underlying cause of the disease is still unclear. However, there are many hypotheses about the cause of Alzheimer’s disease. One theory is the “Amyloid Hypothesis”. This hypothesis involves the presence of the brain protein, beta-amyloid. Beta-amyloid is a sticky compound that accumulates in the brain, eventually disrupting the communication between neurons and killing them. It is believed by researchers that flaws in the biological processes that control the production, disposal, and build-up of beta-amyloid are the primary cause of Alzheimer’s disease. In the Alzheimer’s brain, there is an abnormal amount of beta-amyloid, which can be linked to a larger protein known as the amyloid precursor protein (APP). The function of the APP is not clear; however, a great deal is known about its surroundings. When APP is activated, it is cut by other proteins into smaller sections inside and outside of the cell, and under some circumstances, the smaller sections could be beta-amyloid plaques.
What type of evidence do the researchers have to support the amyloid hypothesis? Firstly, after investigating hundreds of families worldwide, scientists have been able to identify rare genetic mutations that indicate the development of Alzheimer’s disease, and each of these genes is involved in the biological processes of forming and building beta-amyloid protein. Additionally, scientists have also genetically engineered mice in labs to carry these mutations. The mice developed beta-amyloid plaques and began showing symptoms of Alzheimer’s Disease, shown through their inability to navigate through a maze and other human-like symptoms.
Although the amyloid hypothesis has strong evidence supporting it, several clinical trials testing beta-amyloid drugs have been unsuccessful. However, one clinical trial published in 2016 showed evidence that a drug that prevents the accumulation of beta-amyloid reduced beta-amyloid levels and slowed the cognitive decline of patients with Alzheimer’s disease. Currently, the key to treating Alzheimer’s lies in the focus to decrease the production of the protein, whether that means to prevent its accumulation or to increase the removal of the protein. Even though the amyloid hypothesis proves to be a promising answer to the cloudiness around Alzheimer’s disease, researchers believe that there are many different causes of Alzheimer’s, and some even believe that the buildup of beta-amyloid is not the primary cause. Researchers around the world continue to investigate other problems that can lead to the death of neurons and become Alzheimer’s disease.
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