Study of the Aggregation of Amyloid-Beta 40 & 42 in Alzheimer’s Disease

In 1906, Dr. Alois Alzheimer’s diagnosed Auguste Deter with a disease called Alzheimer’s. The disease led to memory loss, dementia, loss of bodily functions, and, eventually, death. Auguste Deter became the first patient to have ever been diagnosed with Alzheimer’s. It was not until the 1970s that Alzheimer’s was considered a major cause of dementia. This led to a boom in research and the discovery of proteins Tau and Amyloid-Beta. Today, 5.4 million people in the United States are diagnosed with Alzheimer’s. In the past century, only a little was discovered about Alzheimer’s. We know that Alzheimer’s is caused by the aggregation of proteins Amyloid-Beta and Tao around neurons but it is still unknown why they aggregate. This study focuses on the aggregation of Amyloid-Beta 40 and 42 under various conditions. The study was presented under the hypothesis that Amyloid-Beta aggregation is a multiphasic, multivariable, process. This was supported through studying different concentrations of Amyloid Beta 40 and 42 in multiple procedures that tested different incubation times, temperatures, concentrations, solvents, etc. The results from the procedures showed that there was a significant difference between the aggregation of AB 40 and 42. Tris seemed to show more successful results than ammonium hydroxide. Each procedure tested different antibodies at different concentration on the same sample. These results could then be used to test future ideas and questions about AB under cellular conditions