ArticleJournal of neuroinflammation2015
An N-terminal antibody promotes the transformation of amyloid fibrils into oligomers and enhances the neurotoxicity of amyloid-beta: the dust-raising effect.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Use of high-affinity scFv antibody NUsc1 for isolation and sensitive detection of Alzheimer's-associated amyloid beta oligomers.The Journal of biological chemistry · 2026Article
- Passive amyloid-β immunotherapy in Alzheimer's disease: a multicellular clearance system beyond plaque removal.Molecular neurodegeneration · 2026Review
- Could the cognitive benefits of amyloid-beta clearance grow in time for Alzheimer's disease?Translational psychiatry · 2026Review
- Targeting phagocytosis for amyloid-β clearance: implications of morphology remodeling and microglia activation probed by bifunctional chimaeras.Nature communications · 2025Article
- Phenotypic alterations in peripheral blood B Lymphocytes of patients with Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2025Article
- Fingolimod ameliorates amyloid deposition and neurodegeneration in APP/PS1 mouse model of Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Article
- GAL-201 as a Promising Amyloid-β-Targeting Small-Molecule Approach for Alzheimer's Disease Treatment: Consistent Effects on Synaptic Plasticity, Behavior and Neuroinflammation.International journal of molecular sciences · 2025Article
- Article
- Autoantibodies to BACE1 promote Aβ accumulation and neurodegeneration in Alzheimer's disease.Acta neuropathologica · 2024Article
- Engineered Antibodies to Improve Efficacy against Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
- Structure of cytotoxic amyloid oligomers generated during disaggregation.Journal of biochemistry · 2024Review
- Article
- AAV-mediated neuronal expression of an scFv antibody selective for Aβ oligomers protects synapses and rescues memory in Alzheimer models.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Antibody-Mediated Clearance of Brain Amyloid-β: Mechanisms of Action, Effects of Natural and Monoclonal Anti-Aβ Antibodies, and Downstream Effects.Journal of Alzheimer's disease reports · 2023Review
- Molecular mechanisms of amyloid disaggregation.Journal of advanced research · 2022Review
- Critical thinking on amyloid-beta-targeted therapy: challenges and perspectives.Science China. Life sciences · 2021Review
- Dreaming of a New World Where Alzheimer's Is a Treatable Disorder.Frontiers in aging neuroscience · 2019Article
- Promising Results from Alzheimer's Disease Passive Immunotherapy Support the Development of a Preventive Vaccine.Research (Washington, D.C.) · 2019Review
- Efficacy and Safety of the Immunization with DNA for Alzheimer's Disease in Animal Models: A Systematic Review from Literature.Journal of Alzheimer's disease reports · 2017Article
- Effective anti-Alzheimer Aβ therapy involves depletion of specific Aβ oligomer subtypes.Neurology(R) neuroimmunology & neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSenile plaques consisting of amyloid-beta (Aβ) are the major pathological hallmark of Alzheimer's disease (AD) and have been the primary therapeutic target. Immunotherapies, which are designed to remove brain Aβ deposits, increased levels of soluble Aβ and accelerated brain atrophy in some clinical trials, suggesting that the solubilization of Aβ deposition might facilitate the formation of more toxic Aβ oligomers and enhance neurotoxicity.
methodsThe capacity of antibodies against different epitopes of Aβ to disaggregate preformed Aβ fibrils was investigated. The co-incubation of antibodies and Aβ fibrils was then tested for neurotoxicity both in vitro and in vivo.
resultsAfter the incubation of preformed Aβ fibrils with the N-terminal antibody 6E10, the fibrils were decreased, while the oligomers, mostly dimers and trimers, were significantly increased. However, no such effects were observed for antibodies targeting the middle domain (4G8) and C-terminus of Aβ (8G7). The co-incubates of preformed Aβ fibrils with 6E10 were more neurotoxic, both in vitro and in vivo, than the co-incubates with 4G8 and 8G7.
conclusionsOur results indicate that the antibody targeting the N-terminus of Aβ promoted the transformation of Aβ from fibrils into oligomers and increased neurotoxicity. Immunotherapies should take into consideration the enhanced neurotoxicity associated with the solubilization of Aβ deposits by antibodies against the Nterminus of Aβ.
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