ArticleJournal of neurochemistry2011
A monoclonal antibody against synthetic Aβ dimer assemblies neutralizes brain-derived synaptic plasticity-disrupting Aβ.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- A genetically encoded selection for amyloid-β oligomer binders.Nature chemical biology · 2025Article
- A Validated Method to Prepare Stable Tau Oligomers.Methods in molecular biology (Clifton, N.J.) · 2023Article
- An ultra-sensitive immunoassay detects and quantifies soluble Aβ oligomers in human plasma.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Emergence of Barrel Motif in Amyloid-β Trimer: A Computational Study.The journal of physical chemistry. B · 2020Article
- Preparation of stable tau oligomers for cellular and biochemical studies.Analytical biochemistry · 2019Article
- The proof-of-concept of ASS234: Peripherally administered ASS234 enters the central nervous system and reduces pathology in a male mouse model of Alzheimer disease.Journal of psychiatry & neuroscience : JPN · 2017Article
- Intrahippocampal administration of a domain antibody that binds aggregated amyloid-β reverses cognitive deficits produced by diet-induced obesity.Biochimica et biophysica acta · 2016Article
- Anti-Aβ antibodies incapable of reducing cerebral Aβ oligomers fail to attenuate spatial reference memory deficits in J20 mice.Neurobiology of disease · 2015Article
- Differential proteomic and behavioral effects of long-term voluntary exercise in wild-type and APP-overexpressing transgenics.Neurobiology of disease · 2015Article
- A human monoclonal IgG that binds aβ assemblies and diverse amyloids exhibits anti-amyloid activities in vitro and in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease.Frontiers in cellular neuroscience · 2015Review
- Amyloid-beta: a crucial factor in Alzheimer's disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2015Review
- mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo.Nature communications · 2014Article
- Naturally occurring autoantibodies interfere with β-amyloid metabolism and improve cognition in a transgenic mouse model of Alzheimer's disease 24 h after single treatment.Translational psychiatry · 2013Article
- Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy.Neuro-degenerative diseases · 2013Article
- Alzheimer's disease Aβ assemblies mediating rapid disruption of synaptic plasticity and memory.Molecular brain · 2012Review
- Aggregation, impaired degradation and immunization targeting of amyloid-beta dimers in Alzheimer's disease: a stochastic modelling approach.Molecular neurodegeneration · 2012Article
- The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes.Nature neuroscience · 2012Review
- Modeling amyloid-beta as homogeneous dodecamers and in complex with cellular prion protein.PloS one · 2012Article
- Human anti-Aβ IgGs target conformational epitopes on synthetic dimer assemblies and the AD brain-derived peptide.PloS one · 2012Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
Diverse lines of evidence indicate that pre-fibrillar, diffusible assemblies of the amyloid β-protein (Aβ) play an important role in Alzheimer's disease pathogenesis. Although the precise molecular identity of these soluble toxins remains unsettled, recent experiments suggest that sodium dodecyl sulfate (SDS)-stable Aβ dimers may be the basic building blocks of Alzheimer's disease-associated synaptotoxic assemblies and as such present an attractive target for therapeutic intervention. In the absence of sufficient amounts of highly pure cerebral Aβ dimers, we have used synthetic disulfide cross-linked dimers (free of Aβ monomer or fibrils) to generate conformation-specific monoclonal antibodies. These dimers aggregate to form kinetically trapped protofibrils, but do not readily form fibrils. We identified two antibodies, 3C6 and 4B5, which preferentially bind assemblies formed from covalent Aβ dimers, but do not bind to Aβ monomer, amyloid precursor protein, or aggregates formed by other amyloidogenic proteins. Monoclonal antibody 3C6, but not an IgM isotype-matched control antibody, ameliorated the plasticity-disrupting effects of Aβ extracted from the aqueous phase of Alzheimer's disease brain, thus suggesting that 3C6 targets pathogenically relevant Aβ assemblies. These data prove the usefulness of covalent dimers and their assemblies as immunogens and recommend further investigation of the therapeutic and diagnostic utility of monoclonal antibodies raised to such assemblies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.