Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss

By Yuesong Gong, Lei Chang, K. Viola, P. Lacor, M. Lambert, C. Finch, G. Krafft, W. Klein. Proceedings of the National Academy of Sciences of the United States of America, 2003

1,118 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/a329c7377cdd17b85f69fa4426a3b5f4ad78b174

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Citations in the corpus

Aβ Oligomers – a decade of discovery (2007, background): “The in vivo relevance of ADDLs is suggested by the finding that antibodies raised to solutions of Ab1–42 that contained monomer and ADDLs produced antibodies (M93 and M94) that prevented Ab-induced toxicity and showed that both synthetic Ab1–42 and some forms of brain-derived Ab bound specifically t”
Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model. (2004, positive): “, 2002) and toxic Aβ oligomer binding at punctate PSD-95-positive sites (Gong et al., 2003) could drive this compartmentalized postsynaptic pathology, which was revealed at the ultrastructural level by focal caspase-cleaved actin (fractin) staining and supported by Western analysis.”
Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “Apparent ADDL-like oligomeric assemblies have been isolated from postmortem AD brains and their presence correlated with memory loss (Gong et al. 2003).”
Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. (2011, background): “This possibility is supported by previous reports (14,19,20,41) in which researchers reported the toxicity of Ab oligomers.”
Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers (2004, methodology): “These antibodies bind to low doses of pathogenic A oligomers but not physiological monomers (Lambert et al., 2001; Chang et al., 2003; Gong et al., 2003) and, as described above, are specific for AD brain tissue.”
Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide (2007, background): “Apparent ADDL-like oligomeric assemblies have been isolated from post-mortem AD brains, and their presence correlated with memory los”
Inflammation, Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease (2014, background): “Oligomers were recently detected at postsynaptic sites in AD hippocampi (47), and their levels are elevated in the brain and cerebrospinal fluid of AD patients (48,49).”
Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers (2009, methodology): “These were prepared from A 1–42 or scrambled A as previously described (1, 11) and detailed in SI Methods.”