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.
Amyloid Beta Peptide and the Amyloid Cascade Hypothesis
Are there alternative approaches to the amyloid cascade hypothesis and what progress has been made?
While there was consensus that the amyloid cascade hypothesis adequately explains the mis-metabolism of amyloid in Alzheimer's Disease, there was concern that both pre-clinical experiments and therapeutic efforts have not borne fruit.
While a comprehensive understanding of ADs pathophysiology is far from complete, several therapeutic approaches based on the amyloid cascade hypothesis of AD with disease-modifying potential are now in late stage clinical trials.
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