ArticleActa neuropathologica communications2018
In vivo induction of membrane damage by β-amyloid peptide oligomers.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- The amino acid substitutions A30W, K28A, and M35C alter amyloid-β peptide toxicity in cell culture and in anFrontiers in aging neuroscience · 2026Article
- Aducanumab binds high molecular weight soluble Aβ oligomers and restores intracellular calcium levels.Alzheimer's research & therapy · 2025Article
- Exploitable mechanisms of antibody and CAR mediated macrophage cytotoxicity.Nature communications · 2025Article
- Enhancing Membrane Repair Using Recombinant MG53/TRIM72 (rhMG53) Reduces Neurotoxicity in Alzheimer's Disease Models.Biomolecules · 2025Article
- Amyloid-β oligomers increase the binding and internalization of tau oligomers in human synapses.Acta neuropathologica · 2024Article
- Plasma membrane repair defect in Alzheimer's disease neurons is driven by the reduced dysferlin expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Hybrid Amyloid Quantum Dot Nano-Bio Assemblies to Probe Neuroinflammatory Damage.ACS chemical neuroscience · 2024Article
- Lipid rafts and human diseases: why we need to target gangliosides.FEBS open bio · 2023Review
- Review
- Applications of Single-Molecule Vibrational Spectroscopic Techniques for the Structural Investigation of Amyloid Oligomers.Molecules (Basel, Switzerland) · 2022Review
- Cholesterol as a key player in amyloid β-mediated toxicity in Alzheimer's disease.Frontiers in molecular neuroscience · 2022Review
- Autophagy Regulation Influences β-Amyloid Toxicity in TransgenicFrontiers in aging neuroscience · 2022Article
- Membrane interaction to intercellular spread of pathology in Alzheimer's disease.Frontiers in neuroscience · 2022Review
- Exogenous misfolded protein oligomers can cross the intestinal barrier and cause a disease phenotype in C. elegans.Scientific reports · 2021Article
- Understanding the Role of Protein Glycation in the Amyloid Aggregation Process.International journal of molecular sciences · 2021Review
- Plasma membrane integrity: implications for health and disease.BMC biology · 2021Review
- Prediction of Transmembrane Regions, Cholesterol, and Ganglioside Binding Sites in Amyloid-Forming Proteins Indicate Potential for Amyloid Pore Formation.Frontiers in molecular neuroscience · 2021Article
- Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in Rats.Drug design, development and therapy · 2021Article
- Neuroprotective Effects of Palmatine via the Enhancement of Antioxidant Defense and Small Heat Shock Protein Expression in AOxidative medicine and cellular longevity · 2021Article
- Viroporins vs. Other Pore-Forming Proteins: What Lessons Can We Take?Frontiers in chemistry · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Exposure to the β-amyloid peptide (Aβ) is toxic to neurons and other cell types, but the mechanism(s) involved are still unresolved. Synthetic Aβ oligomers can induce ion-permeable pores in synthetic membranes, but whether this ability to damage membranes plays a role in the ability of Aβ oligomers to induce tau hyperphosphorylation, or other disease-relevant pathological changes, is unclear. To examine the cellular responses to Aβ exposure independent of possible receptor interactions, we have developed an in vivo C. elegans model that allows us to visualize these cellular responses in living animals. We find that feeding C. elegans E. coli expressing human Aβ induces a membrane repair response similar to that induced by exposure to the CRY5B, a known pore-forming toxin produced by B. thuringensis. This repair response does not occur when C. elegans is exposed to an Aβ Gly37Leu variant, which we have previously shown to be incapable of inducing tau phosphorylation in hippocampal neurons. The repair response is also blocked by loss of calpain function, and is altered by loss-of-function mutations in the C. elegans orthologs of BIN1 and PICALM, well-established risk genes for late onset Alzheimer's disease. To investigate the role of membrane repair on tau phosphorylation directly, we exposed hippocampal neurons to streptolysin O (SLO), a pore-forming toxin that induces a well-characterized membrane repair response. We find that SLO induces tau hyperphosphorylation, which is blocked by calpain inhibition. Finally, we use a novel biarsenical dye-tagging approach to show that the Gly37Leu substitution interferes with Aβ multimerization and thus the formation of potentially pore-forming oligomers. We propose that Aβ-induced tau hyperphosphorylation may be a downstream consequence of induction of a membrane repair process.
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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 OpenQuestion graph.