Does the Amyloid Model of Alzheimer’s Disease Still Make Sense? My Journey to Resolve the Gaps
Whoever can pinpoint the missing piece will be on the verge of solving this seemingly unsolvable disease.
When I was a final-year undergraduate student learning about advanced neurobiology in 2019, I was taught that Alzheimer’s disease (AD) is caused by excessive accumulation of amyloid-beta (Aβ) until it forms toxic plaques in the brain.
I accepted that as a textbook fact. After all, it makes sense that toxic plaques in the brain would trigger neurodegeneration, and, of course, clearing them would solve the problem.
But five years later, after immersing myself in research rather than textbooks, I learned that the amyloid hypothesis of AD isn’t the full story. I learned that science can change and evolve, and sometimes, it takes a 180° flip in reasoning to answer seemingly unsolvable questions.
Other scientists have raised similar doubts about the validity of the amyloid hypothesis of AD in academic papers (Figure 1). In this article, I will re-convey their message, as well as others, in a more comprehensible blog post while also adding my own insights into the matter.
