This is the basis of the amyloid cascade hypothesis
which suggests that the accumulation of A[beta]P results in the pathogenesis of AD [28, 29].
 Hardy and Selkoe proposed the amyloid cascade hypothesis
in later years.
The amyloid cascade hypothesis that A[beta] aggregates form amyloid plaque, neurofibrillary tangle, and lead to neuronal death is one of pathogeneses in AD .
Higgins, "Alzheimer's disease: the amyloid cascade hypothesis," Science, vol.
Based on neuropathological AD hallmarks, the most well-known hypothesis concerning AD pathogenesis is the amyloid cascade hypothesis
, which assumes that a key event in the development of this pathology is an abnormal amyloidogenic cleavage of the transmembrane amyloid precursor protein (APP).
Whereas in the amyloid cascade hypothesis
genetic, pathologic, and biochemical evidence implicate aggregation of A[beta] as a critical early trigger in the chain of events that lead to tauopathy, neuronal dysfunction, and dementia (16), the degree of Tau deposition correlates with the cognitive decline in AD (17,18) questioning the role of A[beta] deposition as the trigger for Tau pathogenesis.
According to the amyloid cascade hypothesis
, A[beta] peptides form aggregates and toxic assemblies which initiate several processes leading to neuronal dysfunction and ultimately large-scale cell death .
This so-called "amyloid cascade hypothesis
" puts beta-amyloid protein at the center of AD pathology.
Formulation of the amyloid cascade hypothesis
proposed by Hardy and Higgins  was the most influential theory to explain why abnormal processing of A[beta] constitutes the underlying mechanism responsible for the progressive development of AD pathogenesis.
Reassessing the amyloid cascade hypothesis
of Alzheimer's disease, int.
"Whether that is due to the study design, or means we need to be rethinking what is going on with the amyloid cascade hypothesis
is an interesting question."