2015
DOI: 10.1093/brain/awv006
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Rapidly progressive Alzheimer’s disease features distinct structures of amyloid-β

Abstract: Genetic and environmental factors that increase the risk of late-onset Alzheimer disease are now well recognized but the cause of variable progression rates and phenotypes of sporadic Alzheimer's disease is largely unknown. We aimed to investigate the relationship between diverse structural assemblies of amyloid-β and rates of clinical decline in Alzheimer's disease. Using novel biophysical methods, we analysed levels, particle size, and conformational characteristics of amyloid-β in the posterior cingulate co… Show more

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Cited by 169 publications
(230 citation statements)
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“…Certain factors can be used to predict RCD, including moderate dementia at the time of treatment onset; vascular risk factors; a younger age; a higher level of education [33]; and the early appearance of hallucinations, psychosis, or extrapyramidal symptoms [34]. Possible biological explanations of variability in the rate of AD-related dementia progression include pathological changes in the blood vessels and the limbic and neocortical structures [35], and (perhaps) the development of distinct amyloid structures [36]. Some evidence indicates that certain genetic biomarkers accelerate the progression of cognitive decline in those with AD-related dementia [37].…”
Section: Discussionmentioning
confidence: 99%
“…Certain factors can be used to predict RCD, including moderate dementia at the time of treatment onset; vascular risk factors; a younger age; a higher level of education [33]; and the early appearance of hallucinations, psychosis, or extrapyramidal symptoms [34]. Possible biological explanations of variability in the rate of AD-related dementia progression include pathological changes in the blood vessels and the limbic and neocortical structures [35], and (perhaps) the development of distinct amyloid structures [36]. Some evidence indicates that certain genetic biomarkers accelerate the progression of cognitive decline in those with AD-related dementia [37].…”
Section: Discussionmentioning
confidence: 99%
“…The existence of variant structural strains of Ab is increasingly well established (Eisenberg and Jucker 2012;Lu et al 2013;Hatami et al 2014;Spirig et al 2014;Cohen et al 2015). Growing evidence supports the hypothesis that Ab seeds, like PrP prions (Aguzzi et al 2007;Collinge and Clarke 2007;Prusiner 2013), can also adopt different molecular conformations that are linked to their functionality in vivo (MeyerLuehmann et al 2006;Eisenberg and Jucker 2012;Stöhr et al 2014;Watts et al 2014).…”
Section: The Interaction Of Ab Strains and Host Factorsmentioning
confidence: 96%
“…Fibrils are polymorphic-Aβ forms fibrils with distinct structures depending on experimental conditions (35,36). Additionally, different fibril types have different impacts on neurodegeneration (26,33,(37)(38)(39). Thus, characterization of the structural dynamics of the fibril formation process is an important endeavor.…”
mentioning
confidence: 99%