Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model
By J. Dodart, K. Bales, K. Gannon, S. Greene, R. DeMattos, C. Mathis, C. Delong, Su Wu, Xin Wu, D. Holtzman and 1 more. Nature Neuroscience, 2002
932 citations recorded by the source corpus.
Subfields: Neurology, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/e49878122779889ff11805b7fae83d5ed8993b1b
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Citations in the corpus
- Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers (2006, background): “Injection of Aβ antibodies into adult APP transgenic mice can rapidly restore synaptic function without overt changes in histopathology (DeMattos et al. 2001; Dodart et al. 2002).”
- Alzheimer's disease: strategies for disease modification (2010, background): “Finally, several studies in transgenic mouse models have observed acute beneficial effects on cognitive performanc”
- Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “Antibodies against A prevent synapse degeneration in Tg mice (Buttini et al., 2005), but memory impairment is reversed without loss of plaques (Dodart et al., 2002; Kotilinek et al., 2002).”
- Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “In addition, our linkage of acute behavioral deficits with soluble oligomers provides a mechanistic explanation for the rapid restoration of cognitive function that followed administration of anti-Aβ antibodies in behaviorally impaired APP transgenic mice (Dodart et al. 2002; Kotilinek et al. 2002).”
- Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers (2004, background): “Studies of experimental vaccines with transgenic (tg) human amyloid protein precursor (hAPP) mice, which provide good models of early AD by developing age-dependent plaques and memory dysfunction (Dodart et al., 2002; Kotilinek et al., 2002), have been particularly illustrative.”
- Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide (2007, background): “and/or the inhibition of Aβ oligomerization and cytotoxicit”
- Alzheimer's disease. (2011, background): “In one study, acute administration of a single injection of an antibody appeared to return certain cognitive deficits to baseline in older mice, obviously without reducing plaque burden (Dodart et al. 2002).”
- Aβ Oligomers – a decade of discovery (2007, background): “Whether LTP is a valid electrophysiological surrogate of learning and memory is still contentious (Dudai 2002).”
- Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, result): “The cognitive deficits in recognition memory do not appear as robust as those in working memory in this model as there are inconsistent reports in the literature (Dodart et al., 1999, 2002; Chen et al., 2000).”