ArticleScientific reports2016
Time-dependent reversal of synaptic plasticity induced by physiological concentrations of oligomeric Aβ42: an early index of Alzheimer's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 64 citations in OpenAlex.
- A phase 2 double-blind placebo-controlled 24-week treatment clinical study of the p38 alpha kinase inhibitor neflamapimod in mild Alzheimer's disease.Alzheimer's research & therapy · 2021Trial
- Neurogenesis and neuroplasticity activities of natural products: therapeutic potential in Alzheimer's disease.Frontiers in pharmacology · 2026Review
- Amyloid-β acute exposition affects the CA1 hippocampal network activity and its topological organization, evaluated with multielectrode arrays.Frontiers in dementia · 2026Article
- Imaging microtubule dynamics: A new frontier in biomarker development for neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Alzheimer disease: Amyloid peptide controversies and challenges of anti-Aβ immunotherapy.The Journal of pharmacology and experimental therapeutics · 2025Review
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Systems-Level Interactome Mapping Reveals Actionable Protein Network Dysregulation Across the Alzheimer's Disease Spectrum.Research square · 2025Article
- Adverse Effects of AβBiomolecules · 2024Article
- Amyloid-β: A potential mediator of aging-related vascular pathologies.Vascular pharmacology · 2023Review
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- The Fuzzy Border between the Functional and Dysfunctional Effects of Beta-Amyloid: A Synaptocentric View of Neuron-Glia Entanglement.Biomedicines · 2023Review
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Early impairment of cortical circuit plasticity and connectivity in the 5XFAD Alzheimer's disease mouse model.Translational psychiatry · 2022Article
- Article
- Miniature neurotransmission is required to maintain Drosophila synaptic structures during ageing.Nature communications · 2021Article
- Heightened Hippocampal β-Adrenergic Receptor Function Drives Synaptic Potentiation and Supports Learning and Memory in the TgF344-AD Rat Model during Prodromal Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Axonal generation of amyloid-β from palmitoylated APP in mitochondria-associated endoplasmic reticulum membranes.Cell reports · 2021Article
- Implications of Oligomeric Amyloid-Beta (oAβThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Age-Related Transcriptional Deregulation of Genes Coding Synaptic Proteins in Alzheimer's Disease Murine Model: Potential Neuroprotective Effect of Fingolimod.Frontiers in molecular neuroscience · 2021Article
- (Dys)regulation of Synaptic Activity and Neurotransmitter Release by β-Amyloid: A Look Beyond Alzheimer's Disease Pathogenesis.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
The oligomeric amyloid-β (Aβ) peptide is thought to contribute to the subtle amnesic changes in Alzheimer's disease (AD) by causing synaptic dysfunction. Here, we examined the time course of synaptic changes in mouse hippocampal neurons following exposure to Aβ42 at picomolar concentrations, mimicking its physiological levels in the brain. We found opposite effects of the peptide with short exposures in the range of minutes enhancing synaptic plasticity, and longer exposures lasting several hours reducing it. The plasticity reduction was concomitant with an increase in the basal frequency of spontaneous neurotransmitter release, a higher basal number of functional presynaptic release sites, and a redistribution of synaptic proteins including the vesicle-associated proteins synapsin I, synaptophysin, and the post-synaptic glutamate receptor I. These synaptic alterations were mediated by cytoskeletal changes involving actin polymerization and p38 mitogen-activated protein kinase. These in vitro findings were confirmed in vivo with short hippocampal infusions of picomolar Aβ enhancing contextual memory and prolonged infusions impairing it. Our findings provide a model for initiation of synaptic dysfunction whereby exposure to physiologic levels of Aβ for a prolonged period of time causes microstructural changes at the synapse which result in increased transmitter release, failure of synaptic plasticity, and memory loss.
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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.