References in periodicals archive
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1] Hardy and Selkoe proposed the amyloid cascade hypothesis in later years.
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].
Although the exact cause of AD is still a matter of debate, the amyloid cascade hypothesis is the best accepted and most studied hypothesis among those mentioned above.
In the early 1990s, it was proposed that the main essence of the amyloid cascade hypothesis is increased production or decreased clearance of A[beta] peptide, the culprit behind AD [39,40].
The leading amyloid cascade hypothesis for the pathogenesis of AD states that amyloid-E- (AE-) starts to accumulate
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.
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