ArticleMolecular brain2017
The neurotoxicity of amyloid β-protein oligomers is reversible in a primary neuron model.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Neuroprotective Potency of Neolignans inFrontiers in pharmacology · 2022Pooled it
- Targeting gangliosides to treat Alzheimer's and Parkinson's diseases: A disruptive approach with the first-in-class peptide AmyP53.Neural regeneration research · 2026Article
- Clusterin induced by OPC phagocytosis blocks IL-9 secretion to inhibit myelination in a model of Alzheimer's disease.Heliyon · 2025Article
- Chemical Composition, In Vivo, and In Silico Molecular Docking Studies of the Effect ofPlants (Basel, Switzerland) · 2025Article
- The Interplay Between Accumulation of Amyloid-Beta and Tau Proteins, PANoptosis, and Inflammation in Alzheimer's Disease.Neuromolecular medicine · 2024Review
- Design, synthesis, and evaluation of 2,2'-bipyridyl derivatives as bifunctional agents against Alzheimer's disease.Molecular diversity · 2024Article
- Possible Role of Fibrinaloid Microclots in Postural Orthostatic Tachycardia Syndrome (POTS): Focus on Long COVID.Journal of personalized medicine · 2024Article
- Neuroprotective Effect of Solid Lipid Nanoparticles Loaded withNanomaterials (Basel, Switzerland) · 2024Article
- Activation of Lysosomal Function Ameliorates Amyloid-β-Induced Tight Junction Disruption in the Retinal Pigment Epithelium.Molecules and cells · 2023Article
- In Vivo Preclinical Assessment of β-Amyloid-Affine [International journal of molecular sciences · 2022Article
- Screening neuroprotective compounds in herpes-induced Alzheimer's disease cell and 3D tissue models.Free radical biology & medicine · 2022Review
- Nonapoptotic caspases in neural development and in anesthesia-induced neurotoxicity.Trends in neurosciences · 2022Review
- Administration of mucuna beans (Mucuna pruriences (L.) DC. var. utilis) improves cognition and neuropathology of 3 × Tg-AD mice.Scientific reports · 2022Article
- Protection against Amyloid-β Oligomer Neurotoxicity by Small Molecules with Antioxidative Properties: Potential for the Prevention of Alzheimer's Disease Dementia.Antioxidants (Basel, Switzerland) · 2022Review
- An Alzheimer's Disease Mechanism Based on Early Pathology, Anatomy, Vascular-Induced Flow, and Migration of Maximum Flow Stress Energy Location with Increasing Vascular Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Mitigating Effect of Estrogen in Alzheimer's Disease-Mimicking Cerebral Organoid.Frontiers in neuroscience · 2022Article
- TREM2 modulates differential deposition of modified and non-modified Aβ species in extracellular plaques and intraneuronal deposits.Acta neuropathologica communications · 2021Article
- Autoxidation Enhances Anti-Amyloid Potential of Flavone Derivatives.Antioxidants (Basel, Switzerland) · 2021Article
- Mild magnetic nanoparticle hyperthermia promotes the disaggregation and microglia-mediated clearance of beta-amyloid plaques.Nanomedicine : nanotechnology, biology, and medicine · 2021Article
- An explicitly designed paratope of amyloid-β prevents neuronal apoptosisChemical science · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by the accumulation of extracellular amyloid β-protein (Aβ) and intracellular hyperphosphorylated tau proteins. Recent evidence suggests that soluble Aβ oligomers elicit neurotoxicity and synaptotoxicity, including tau abnormalities, and play an initiating role in the development of AD pathology. In this study, we focused on the unclarified issue of whether the neurotoxicity of Aβ oligomers is a reversible process. Using a primary neuron culture model, we examined whether the neurotoxic effects induced by 2-day treatment with Aβ42 oligomers (Aβ-O) are reversible during a subsequent 2-day withdrawal period. Aβ-O treatment resulted in activation of caspase-3 and eIF2α, effects that were considerably attenuated following Aβ-O removal. Immunocytochemical analyses revealed that Aβ-O induced aberrant phosphorylation and caspase-mediated cleavage of tau, both of which were mostly reversed by Aβ-O removal. Furthermore, Aβ-O caused intraneuronal dislocation of β-catenin protein and a reduction in its levels, and these alterations were partially reversed upon Aβ-O withdrawal. The dislocation of β-catenin appeared to reflect synaptic disorganization. These findings indicate that removal of extracellular Aβ-O can fully or partially reverse Aβ-O-induced neurotoxic alterations in our neuron model. Accordingly, we propose that the induction of neurotoxicity by Aβ oligomers is a reversible process, which has important implications for the development of AD therapies.
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Registered trials
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