The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal

By John Hardy. Journal of Neurochemistry, 2009

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Prevalence of Amyloid PET Positivity in Dementia Syndromes (2015, neutral): “APOE ε4 noncarrier 18 29 (15-50) 54 (30-77)”
Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer's disease. (2016, background): “, 2015) will for the first time allow indepth testing of the entire amyloid cascade hypothesis (Hardy, 2009) in vivo.”
A review on Alzheimer’s disease pathophysiology and its management: an update (2015, background): “for the complex pathophysiology of this incapacitating disease [8].”
Genetic Evidence Implicates the Immune System and Cholesterol Metabolism in the Aetiology of Alzheimer's Disease (2010, background): “Nevertheless these findings do not exclude a central role for the amyloid cascade [5] in pathogenesis, and indeed, both processes highlighted by our analysis have been implicated in Ab clearance in the brain [40] though further work is required to determine whether the risk these processes confer is”
Brain-wide pathway for waste clearance captured by contrast-enhanced MRI. (2013, positive): “In our prior study (6), we reported that the glymphatic pathway is an important contributor to the clearance of interstitial solutes such as soluble amyloid β , a peptide widely believed to be a critical driver of AD pathogenesis (15, 16).”