ArticlePloS one2010
Synaptotoxicity of Alzheimer beta amyloid can be explained by its membrane perforating property.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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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
72 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Membrane Pore Formation by Peptides Studied by Fluorescence Techniques.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Pathological calcium influx through amyloid beta pores disrupts synaptic function.Cell calcium · 2025Article
- An Expanded Narrative Review of Neurotransmitters on Alzheimer's Disease: The Role of Therapeutic Interventions on Neurotransmission.Molecular neurobiology · 2025Review
- Impacts of CACNB4 overexpression on dendritic spine density in both sexes and relevance to schizophrenia.Translational psychiatry · 2024Article
- Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.Nature communications · 2024Article
- Loss of glycine receptors in the nucleus accumbens and ethanol reward in an Alzheimer´s Disease mouse model.Progress in neurobiology · 2024Article
- The structure of tyrosine-10 favors ionic conductance of Alzheimer's disease-associated full-length amyloid-β channels.Nature communications · 2024Article
- Rigidifying of the internal dynamics of amyloid-beta fibrils generated in the presence of synaptic plasma vesicles.Physical chemistry chemical physics : PCCP · 2024Article
- Neuroprotective Properties of Eudesmin on a Cellular Model of Amyloid-β Peptide Toxicity.Journal of Alzheimer's disease : JAD · 2023Article
- Endogenous Amyloid-formed CaFunction (Oxford, England) · 2023Article
- Sleep-controlling neurons are sensitive and vulnerable to multiple forms of α-synuclein: implications for the early appearance of sleeping disorders in α-synucleinopathies.Cellular and molecular life sciences : CMLS · 2022Article
- Molecular insights into the primary nucleation of polymorphic amyloid β dimers in DOPC lipid bilayer membrane.Protein science : a publication of the Protein Society · 2022Article
- Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions.Molecules (Basel, Switzerland) · 2022Review
- Effects of Aβ-derived peptide fragments on fibrillogenesis of Aβ.Scientific reports · 2021Article
- Protective Role of a Donepezil-Huprine Hybrid against the β-Amyloid (1-42) Effect on Human Erythrocytes.International journal of molecular sciences · 2021Article
- Ultrasmall Molybdenum Disulfide Quantum Dots Cage Alzheimer's Amyloid Beta to Restore Membrane Fluidity.ACS applied materials & interfaces · 2021Article
- Review
- Expression of N-Terminal Cysteine AβBiochemistry · 2021Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms that induce Alzheimer's disease (AD) are largely unknown thereby deterring the development of disease-modifying therapies. One working hypothesis of AD is that Abeta excess disrupts membranes causing pore formation leading to alterations in ionic homeostasis. However, it is largely unknown if this also occurs in native brain neuronal membranes. Here we show that similar to other pore forming toxins, Abeta induces perforation of neuronal membranes causing an increase in membrane conductance, intracellular calcium and ethidium bromide influx. These data reveal that the target of Abeta is not another membrane protein, but that Abeta itself is the cellular target thereby explaining the failure of current therapies to interfere with the course of AD. We propose that this novel effect of Abeta could be useful for the discovery of anti AD drugs capable of blocking these "Abeta perforates". In addition, we demonstrate that peptides that block Abeta neurotoxicity also slow or prevent the membrane-perforating action of Abeta.
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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.