ArticleScience signaling2017
The amyloid-β oligomer Aβ*56 induces specific alterations in neuronal signaling that lead to tau phosphorylation and aggregation.
Article in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 108 citations in OpenAlex.
- Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026Review
- Morphological and Molecular Profiling of Amyloid-β Species in Alzheimer's Pathogenesis.Molecular neurobiology · 2025Review
- Long-term gabapentin treatment impairs cognitive function in aged mice via tau hyperphosphorylation.Frontiers in pharmacology · 2025Article
- Oligomeric Amyloid-β and Tau Alter Cell Adhesion Properties and Induce Inflammatory Responses in Cerebral Endothelial Cells Through the RhoA/ROCK Pathway.Molecular neurobiology · 2024Article
- Selective disruption of synaptic NMDA receptors of the hippocampal trisynaptic circuit in Aβ pathology.Biological research · 2024Article
- Antibodies Raised Against an Aβ Oligomer Mimic Recognize Pathological Features in Alzheimer's Disease and Associated Amyloid-Disease Brain Tissue.ACS central science · 2024Article
- Binding mechanism of full-length Aβ40 peptide to a mixed lipid bilayer.Frontiers in chemistry · 2024Article
- 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
- Brain targeting based nanocarriers loaded with resveratrol in Alzheimer's disease: A review.IET nanobiotechnology · 2023Review
- A Function of Amyloid-β in Mediating Activity-Dependent Axon/Synapse Competition May Unify Its Roles in Brain Physiology and Pathology.Journal of Alzheimer's disease : JAD · 2023Review
- SOBA: Development and testing of a soluble oligomer binding assay for detection of amyloidogenic toxic oligomers.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Treadmill Exercise Reduces Neuroinflammation, Glial Cell Activation and Improves Synaptic Transmission in the Prefrontal Cortex in 3 × Tg-AD Mice.International journal of molecular sciences · 2022Article
- Comment on "Activation of the Omega-3 Fatty Acid Receptor GPR120 Protects against Focal Cerebral Ischemic Injury by Preventing Inflammation and Apoptosis in Mice".Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Anti-Inflammatory Activity of 4-(4-(Heptyloxy)phenyl)-2,4-dihydro-3Molecules (Basel, Switzerland) · 2022Article
- Synaptic Disruption by Soluble Oligomers in Patients with Alzheimer's and Parkinson's Disease.Biomedicines · 2022Review
- History in Perspective: The prime pathological players and role of phytochemicals in Alzheimer's disease.IBRO neuroscience reports · 2022Review
- Delivery of Intravenously Administered Antibodies Targeting Alzheimer's Disease-Relevant Tau Species into the Brain Based on Receptor-Mediated Transcytosis.Pharmaceutics · 2022Review
- Novel Stilbene-Nitroxyl Hybrid Compounds Display Discrete Modulation of Amyloid Beta Toxicity and Structure.Frontiers in chemistry · 2022Article
- Review
- Death-associated protein kinase 1 mediates Aβ42 aggregation-induced neuronal apoptosis and tau dysregulation in Alzheimer's disease.International journal of biological sciences · 2022Article
Corrections and comments
- Expression of concern
- RetractedRetraction.2025
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Oligomeric forms of amyloid-forming proteins are believed to be the principal initiating bioactive species in many neurodegenerative disorders, including Alzheimer's disease (AD). Amyloid-β (Aβ) oligomers are implicated in AD-associated phosphorylation and aggregation of the microtubule-associated protein tau. To investigate the specific molecular pathways activated by different assemblies, we isolated various forms of Aβ from Tg2576 mice, which are a model for AD. We found that Aβ*56, a 56-kDa oligomer that is detected before patients develop overt signs of AD, induced specific changes in neuronal signaling. In primary cortical neurons, Aβ*56 interacted with
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What OpenQuestion holds
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.