The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics

By E. Karran, M. Mercken, B. de Strooper. Nature reviews. Drug discovery, 2011

2,139 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/768c4e6d5a35d4c42b704fdea703865e0c951ca7

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Citations in the corpus

Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, neutral): “Unfortunately, many clinical trials have been inadequately designed to robustly test the amyloid hypothesis, such that negative trial results cannot be necessarily interpreted as a rejection of the amyloid hypothesis (Karran and Hardy, 2014; Karran et al., 2011).”
Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012, background): “In sum, clinical trials have not provided deﬁnitive answers as to the direct role of A A Ps or tangles in the cognitive impairment associated with AD pathologic diagnosis (80, 81).”
Cholinesterase inhibitors as Alzheimer's therapeutics (2019, background): “The progressive synthesis and aggregation of β -amyloid (a β ), a proteolytic fragment derived from amyloid precursor protein (aPP), are additional critical factors involved in ad pathogenesis (7).”
Oxidative stress and the amyloid beta peptide in Alzheimer’s disease (2017, background): “The mutations are divided in three categories: mutations at the β-secretase cleavage site (N-term), at the γ-secretase cleavage site (C-term) and in the mid-domain amyloid-β region [29].”
The Major Risk Factors for Alzheimer’s Disease: Age, Sex, and Genes Modulate the Microglia Response to Aβ Plaques (2019, background): “One possible resolution is that amyloid pathology acts only as a trigger in sporadic AD (Karran et al., 2011); i.”
Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, result): “The data also support the “Amyloid Cascade Hypothesis”(Karran et al., 2011), a deceptively complex hypothesis which posits that beta-amyloid/plaque pathology kin-dles widespread tau/NFT pathology, with the tau/NFT pathology constituting the more direct cause of the cell loss and synapse elimination ”
Alzheimer’s disease prevention: from risk factors to early intervention (2017, background): “Cerebral Aβ deposition is considered a necessary, but not sufficient, step on the path towards AD development [44].”