ArticlePloS one2017
In situ fibrillizing amyloid-beta 1-42 induces neurite degeneration and apoptosis of differentiated SH-SY5Y cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
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- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
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- Disruption of Copper Redox Balance and Dysfunction underEnvironment & health (Washington, D.C.) · 2025Article
- Neuroprotective Effects of Dehydroepiandrosterone Sulphate Against Aβ Toxicity and Accumulation in Cellular and Animal Model of Alzheimer's Disease.Biomedicines · 2025Article
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- Targeting necroptosis in Alzheimer's disease: can exercise modulate neuronal death?Frontiers in aging neuroscience · 2025Review
- Effect of Low-Frequency, Low-Energy Pulsed Electromagnetic Fields in Neuronal and Microglial Cells Injured with Amyloid-Beta.International journal of molecular sciences · 2024Article
- Different amyloid β42 preparations induce different cell death pathways in the model of SH-SY5Y neuroblastoma cells.Cellular & molecular biology letters · 2024Article
- Liposomal Formulations of Anti-Alzheimer Drugs and siRNA for Nose-to-Brain Delivery: Design, Safety and Efficacy In Vitro.The AAPS journal · 2024Article
- Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging.Nature communications · 2024Article
- The AβFrontiers in cellular neuroscience · 2024Article
- Ganglioside GM1 produces stable, short, and cytotoxic AβChemical communications (Cambridge, England) · 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
- Protective Role of an Extract Waste Product fromPlants (Basel, Switzerland) · 2023Article
- GLUT inhibitor WZB117 induces cytotoxicity with increased production of amyloid-beta peptide in SH-SY5Y cells preventable by beta-hydroxybutyrate: implications in Alzheimer's disease.Pharmacological reports : PR · 2023Article
- Identification of a Novel Wnt Antagonist Based Therapeutic and Diagnostic Target for Alzheimer's Disease Using a Stem Cell-Derived Model.Bioengineering (Basel, Switzerland) · 2023Article
- Perphenazine-Macrocycle Conjugates Rapidly Sequester the Aβ42 Monomer and Prevent Formation of Toxic Oligomers and Amyloid.ACS chemical neuroscience · 2023Article
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Authors and funding
5 authors.
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Abstract
The progression of Alzheimer's disease is causatively linked to the accumulation of amyloid-β aggregates in the brain, however, it is not clear how the amyloid aggregates initiate the death of neuronal cells. The in vitro toxic effects of amyloid peptides are most commonly examined using the human neuroblastoma derived SH-SY5Y cell line and here we show that differentiated neuron-like SH-SY5Y cells are more sensitive to amyloid peptides than non-differentiated cells, because the latter lack long neurites. Exogenous soluble amyloid-β 1-42 covered cell bodies and whole neurites in differentiated cells with dense fibrils, causing neurite beading and fragmentation, whereas preformed amyloid-β 1-42 fibrils had no toxic effects. Importantly, spontaneously fibrillizing amyloid-β 1-42 peptide exhibited substantially higher cellular toxicity than amyloid-β 1-40, which did not form fibrils under the experimental conditions. These results support the hypothesis that peptide toxicity is related to the active fibrillization process in the incubation mixture.
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