Author(s) :

Ryan Verma.

Volume/Issue :

Abstract :

The amyloid-β cascade hypothesis has served for decades as the foremost explanation for the pathology of Alzheimer’s disease, and it has served as the basis for much research on the mechanisms of and treatments for Alzheimer’s, fostering countless discoveries in the field. This paper will review the historical and current evidence both in support of and challenging the amyloid cascade hypothesis to determine its applicability in modern research. More modern variations of the hypothesis acknowledge the importance of other factors and focus on the role of soluble amyloid oligomers have been able to explain many criticisms of the hypothesis, such as the presence of plaques in healthy individuals, and the weak correlation with cognitive decline, and additionally support has come from new amyloid-targeting drugs. However, while amyloid-β likely plays some role in Alzheimer’s pathology, evidence suggests that amyloid-β alone does not incite pathogenesis. Instead, Alzheimer’s results from a great variety of factors of which amyloid-β may be one, though it is far from being fully understood.