T1 - Perspectives on the Amyloid-β Cascade Hypothesis

N2 - For the better part of the past two decades, studies on the molecular, biochemical and cellular mechanisms of Alzheimer disease have focused on amyloid-β protein, the major proteinaceous component of senile plaques. In fact, the Amyloid Cascade Hypothesis has come to dominate the field both in terms of proposed disease mechanism as well as potential for therapeutic intervention. In this review, we look at the Amyloid Cascade Hypothesis from the perspective of pathology, cell biology, and genetics. In all cases, alternate interpretations of old data as well as new evidence indicates that amyloid-β far from being the harbinger of disease, actually occurs secondary to more fundamental pathological changes and may even play a protective role in the diseased brain. These findings bring into serious doubt the validity of the Amyloid Cascade Hypothesis as the central cause of Alzheimer disease and, consequently, the potential usefulness of therapeutic targets against amyloid-β.

The Amyloid Cascade Hypothesis of Alzheimer's Disease?

T1 - Reassessing the amyloid cascade hypothesis of Alzheimer's disease

Amyloid Cascade Hypothesis and Alzheimer's Disease - …

Dutch forum; Amyloidosis Foundation; Bacterial Inclusion Bodies Contain Amyloid-Like Structure outlines for argumentative essays at SciVee; Amyloid Cascade Hypothesis; the amyloid cascade hypothesis Stanford.

Alzheimer's disease: the amyloid cascade hypothesis | Science

104760 - amyloid beta a4 precursor protein; app - amyloid of aging and alzheimer disease; aaa;; cerebral vascular the amyloid cascade hypothesis amyloid peptide; cvap;; protease.

Bateman, M.D., Chengjie Xiong, Ph., the amyloid cascade hypothesis Tammie L.S.
It is not a prediction of the amyloid cascade hypothesis that the amount of amyloid deposition would correlate with the degree of dementia.

Wrong on So Many Fronts: The Amyloid Cascade Hypothesis

As a new professor at the University of Washington, Paine tested the green world hypothesis. The idea for a simple experiment that essentially involved playing God in the rocky intertidal zone came to him during a visit to the Scripps Institution Wharf in California, as he stood watching the carnivorous sea star Pisaster ochraceus devour the mussel Mytilus californianus. What if he removed sea stars to see what would happen? The next year, National Science Foundation funding in hand, he settled into the University of Washington and began his research. Month after month he traveled to Mukkaw Bay, at the northern tip of the Olympic Peninsula. There, on a rocky crescent of shore, he hurled sea stars into the ocean. In his control plot he did nothing. As he continued removing stars, the assemblage of species on the rocks gradually began to change. Within one year the sinister implications of his experiment became all too graphically obvious. Where Pisaster flourished, so did the vegetation. Where Pisaster had been removed, the mussels took over, crowding out other species and eating all the vegetation, until little more than a dark carpet of mussels and barnacles remained. The paper Paine produced for the American Naturalist about this research turned out to be one of the most influential journal articles in the history of ecology. It provided one of the first examples of an ecosystem that had been transformed by trophic cascades.

Clinical trial results thus far do not support the amyloid cascade hypothesis, but the results also are not a refutation of the hypothesis.

sporadic AD a “mitochondrial cascade hypothesis” that ..

The linkage between fibrils and disease thus was established, both clinically and in vitro, a linkage that came to be known as the ‘amyloid cascade hypothesis’ [].If amyloid fibrils were the proximate neurotoxins in AD, then a reasonable therapeutic approach would be to target fibril formation.

THE AMYLOID CASCADE HYPOTHESIS  The molecular mechanisms and hypotheses of Alzheimer's Disease (AD) can be incredibly complex.

The Amyloid Cascade Hypothesis - UW Milk Quality

For the better part of the past two decades, studies on the molecular, biochemical and cellular mechanisms of Alzheimer disease have focused on amyloid-β protein, the major proteinaceous component of senile plaques. In fact, the Amyloid Cascade Hypothesis has come to dominate the field both in terms of proposed disease mechanism as well as potential for therapeutic intervention. In this review, we look at the Amyloid Cascade Hypothesis from the perspective of pathology, cell biology, and genetics. In all cases, alternate interpretations of old data as well as new evidence indicates that amyloid-β far from being the harbinger of disease, actually occurs secondary to more fundamental pathological changes and may even play a protective role in the diseased brain. These findings bring into serious doubt the validity of the Amyloid Cascade Hypothesis as the central cause of Alzheimer disease and, consequently, the potential usefulness of therapeutic targets against amyloid-β.