2010
DOI: 10.1073/pnas.0914251107
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Abstract: Full-length amyloid beta peptides (Aβ 1-40/42 ) form neuritic amyloid plaques in Alzheimer's disease (AD) patients and are implicated in AD pathology. However, recent transgenic animal models cast doubt on their direct role in AD pathology. Nonamyloidogenic truncated amyloid-beta fragments and Aβ ) are also found in amyloid plaques of AD and in the preamyloid lesions of Down syndrome, a model system for early-onset AD study. Very little is known about the structure and activity of these smaller peptides, alt… Show more

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Cited by 209 publications
(382 citation statements)
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“…Recent evidence suggests an alternative mechanism of A␤ toxicity mediated by the p3 fragment (Jang et al, 2010) interacting with the neuronal membrane and forming Zn-dependent channels. In such a model, cell membranes appear to act as two-dimensional aggregation templates.…”
Section: Discussionmentioning
confidence: 99%
“…Recent evidence suggests an alternative mechanism of A␤ toxicity mediated by the p3 fragment (Jang et al, 2010) interacting with the neuronal membrane and forming Zn-dependent channels. In such a model, cell membranes appear to act as two-dimensional aggregation templates.…”
Section: Discussionmentioning
confidence: 99%
“…The interaction also appears to be important for membrane-associated Aβ assembly into higher ordered structures (Friedman et al, 2009;Sureshbabu et al, 2010). Compromised membrane integrity greatly increases membrane conductance that has been attributed to a putative ionic channel formed by Aβ peptides (Jang et al, 2010). Aβ 1-42 expressed in Drosophila brains induces a deterioration and compromise of autophagylysosomal vesicles ).…”
Section: Lysosome-derived Chemical Lesions and Subcellular Damagementioning
confidence: 99%
“…In other words, mutated SOD1 may be involved in extra-cellular events directly affecting other cells, as previously shown on microglia (6). Growing evidence in support of a toxic channel hypothesis also for Alzheimer's disease and other neurodegenerative diseases lends credence to a common disease mechanism in protein misfolding diseases (7,8). Consistent with this scenario, altered levels of intracellular calcium (Ca 2+ ) are reported to contribute to the motor neuron degeneration and mitochondrial dysfunction associated with ALS (9-12).…”
Section: Introductionmentioning
confidence: 82%