ArticleJournal of neurochemistry2019
A novel crosslinking protocol stabilizes amyloid β oligomers capable of inducing Alzheimer's-associated pathologies.
Article in Journal of neurochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 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
- Targeting soluble misfolded oligomers in anti-amyloid research.Nature reviews. Chemistry · 2026Review
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Threshold Effects of Maternal Vitamin C in Late Pregnancy on Infant Social Competence: A Nonlinear Dose-Response Analysis in a Birth Cohort.Food science & nutrition · 2026Article
- Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases.Molecular neurodegeneration · 2024Review
- EPR Studies of Aβ42 Oligomers Indicate a Parallel In-Register β-Sheet Structure.ACS chemical neuroscience · 2024Article
- Pharmacological inhibition of plasminogen activator inhibitor-1 prevents memory deficits and reduces neuropathology in APP/PS1 mice.Psychopharmacology · 2023Article
- Probing differences among Aβ oligomers with two triangular trimers derived from Aβ.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mass spectrometric insights into protein aggregation.Essays in biochemistry · 2023Review
- Dityrosine cross-linking and its potential roles in Alzheimer's disease.Frontiers in neuroscience · 2023Review
- The Therapeutic and Diagnostic Potential of Amyloid β Oligomers Selective Antibodies to Treat Alzheimer's Disease.Frontiers in neuroscience · 2021Article
- Antibody Fragments as Tools for Elucidating Structure-Toxicity Relationships and for Diagnostic/Therapeutic Targeting of Neurotoxic Amyloid Oligomers.International journal of molecular sciences · 2020Review
- Half a century of amyloids: past, present and future.Chemical Society reviews · 2020Review
- Sodium tanshinone IIA sulfonate protects against Aβ-induced cell toxicity through regulating Aβ process.Journal of cellular and molecular medicine · 2020Article
- In Situ Structural Restraints from Cross-Linking Mass Spectrometry in Human Mitochondria.Journal of proteome research · 2020Article
- Aβ oligomer induced cognitive impairment and evaluation of ACU193-MNS-based MRI in rabbit.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Promising Results from Alzheimer's Disease Passive Immunotherapy Support the Development of a Preventive Vaccine.Research (Washington, D.C.) · 2019Review
- Using mass spectrometry-based methods to understand amyloid formation and inhibition of alpha-synuclein and amyloid beta.Mass spectrometry reviewsReview
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Amyloid β oligomers (AβOs) accumulate early in Alzheimer's disease (AD) and experimentally cause memory dysfunction and the major pathologies associated with AD, for example, tau abnormalities, synapse loss, oxidative damage, and cognitive dysfunction. In order to develop the most effective AβO-targeting diagnostics and therapeutics, the AβO structures contributing to AD-associated toxicity must be elucidated. Here, we investigate the structural properties and pathogenic relevance of AβOs stabilized by the bifunctional crosslinker 1,5-difluoro-2,4-dinitrobenzene (DFDNB). We find that DFDNB stabilizes synthetic Aβ in a soluble oligomeric conformation. With DFDNB, solutions of Aβ that would otherwise convert to large aggregates instead yield solutions of stable AβOs, predominantly in the 50-300 kDa range, that are maintained for at least 12 days at 37°C. Structures were determined by biochemical and native top-down mass spectrometry analyses. Assayed in neuronal cultures and i.c.v.-injected mice, the DFDNB-stabilized AβOs were found to induce tau hyperphosphorylation, inhibit choline acetyltransferase, and provoke neuroinflammation. Most interestingly, DFDNB crosslinking was found to stabilize an AβO conformation particularly potent in inducing memory dysfunction in mice. Taken together, these data support the utility of DFDNB crosslinking as a tool for stabilizing pathogenic AβOs in structure-function studies.
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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 Socratic graph.