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.
References in periodicals archive ?
The leading amyloid cascade hypothesis for the pathogenesis of AD states that amyloid-E- (AE-) starts to accumulate
It is important to note, however, that the recent developments regarding tau protein research which has been widely reported in the media, including in the New York Times in August, do not at all diminish the importance of beta amyloid or teach away from the amyloid cascade hypothesis which postulates that formation of beta amyloid is the critical step in driving Alzheimer's disease 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.
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.
The amyloid cascade hypothesis proposes that certain forms of the ABeta peptide are toxic and causally related to the severity of AD.
The amyloid cascade hypothesis proposes that certain forms of A(B) peptide are toxic and causally related to the severity of AD.
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