A specific amyloid-beta protein assembly in the brain impairs memory.

By Sylvain E. Lesné, M. T. Koh, L. Kotilinek, R. Kayed, C. Glabe, A. Yang, M. Gallagher, K. Ashe. Nature, 2006

1,267 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/182594d1056a20af61859c0eff065e68abcb3cad

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. D. Selkoe
2. P. Lacor
3. D. Walsh
4. C. Parsons
5. Maria C. F. Buniel
6. E. Mandelkow
7. K. Viola
8. P. Velasco

Citations in the corpus

• Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers (2009, background): “The pathological relevance of ADDLs has been substantiated by their disease-specific accumulation in human brain and CSF (1, 22) and by the accumulation of structurally equivalent oligomers in transgenic mouse AD models (23).”
• Aβ Oligomers – a decade of discovery (2007, background): “…performance in a hippocampaldependent contextual fear conditioning assay, decreased spine density in the dentate gyrus, and impairment of long-term potentiation (LTP) at ages long before the first apparent detection of Ab dodecamer (Dineley et al. 2002; Jacobsen et al. 2006; Lesne et al. 2006).”
• The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy (2016, background): “Soluble Aβ oligomers have been reported in AD to be organized into different structures ranging from dimers (Walsh et al., 2000), trimers (Walsh et al., 2000; Chen and Glabe, 2006), tetramers (Walsh et al., 2000; Chen and Glabe, 2006), pentamers and decamers (Ahmed et al., 2010), Aβ-derived diffusib”
• An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers. (2012, unknown): “A β Os increasingly appear to be the proximal toxins that cause synapse failure in AD (12, 13, 24, 25).”
• Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “Aβ oligomers produced by cultured cells could be related to the recently described Aβ*56 species, which represents a soluble, SDS-stable dodecamer found in the brains of at least some APP transgenic mouse lines (Lesne et al. 2006).”
• Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “With respect to size, these synaptotoxic oligomeric ligands are consistent with the prominent 12-mers found in AD brain (Gong et al., 2003) and with a 56 kDa A species reported for a Tg AD mouse model (Lesne et al., 2006).”
• Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines (2010, background): “We also note that in our preparations we did not consistently observe a band at 56 kDa, a species that has been reported to be toxic for transgenic mice (Lesné et al., 2006) but can be visualized in certain conditions (Walsh et al., 2005; Ashe, 2006; Bernstein et al., 2009).”
• Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system--too little activation is bad, too much is even worse. (2007, background): “Amyloid beta (Aß) is the principal constituent of senile plaques in AD and is believed to impair neuronal function and cognition, even before the appearance of overt toxicity (Lesne et al., 2006).”
• Advancing translational research with the Semantic Web (2007, background): “One recent hypothesis on the cause of AD [4] illustrates the typical situation.”
• Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain (2009, background): “While demonstrating neuroinflammatory profiles reminiscent of humans with AD, mouse models of AD show minimal neuronal loss even when levels of toxic Aβ species are high (Lesne et al. 2006; Jimenez et al. 2008; Radde et al. 2008).”
• Islet amyloid polypeptide, islet amyloid, and diabetes mellitus. (2011, background): “However, evidence of soluble oligomers has been obtained from extracts of the brain of Alzheimer-model mice (208) and recently also from human brain tissue (355).”