amyloid cascade hypothesis

amyloid cascade hypothesis

A theoretical explanation of Alzheimer’s disease, which holds that the primary event is the intercellular deposition of Abeta amyloid, which leads to the signs and symptoms of brain damage.
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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].
[1] 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 [29].
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 [7].
The leading amyloid cascade hypothesis for the pathogenesis of AD states that amyloid-E- (AE-) starts to accumulate
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 [29] 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.
"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."
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