Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease

By F. Kametani, M. Hasegawa. Frontiers in Neuroscience, 2018

716 citations recorded by the source corpus.

The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid β (Aβ) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. However, all attempts to develop Aβ-targeting drugs to treat AD have ended in failure. Here, we review recent findings indicating that the main factor underlying the development and progression of AD is tau, not Aβ, and we describe the deficiencies of the amyloid hypothesis that have supported the emergence of this idea.

Subfields: Computational Theory and Mathematics, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/958679c0420b7d94fa2f79529456e4710f929f86

Citations in the corpus

• Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease. (2020, neutral): “The data demonstrate that amyloid plaques are not innocent bystanders of the disease as has been sometimes suggested (Robakis, 2010; Kametani and Hasegawa, 2018), but are in fact inducing a strong and coordinated response of all cell types in the amyloid plaque cellular niche (De Strooper and Karran”