ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Effect of Aβ Oligomers on Neuronal APP Triggers a Vicious Cycle Leading to the Propagation of Synaptic Plasticity Alterations to Healthy Neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
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- Alzheimer disease: Amyloid peptide controversies and challenges of anti-Aβ immunotherapy.The Journal of pharmacology and experimental therapeutics · 2025Review
- CD2AP at the junction of nephropathy and Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Familial Alzheimer's disease mutations in amyloid precursor protein impair calcineurin signaling to NMDA receptors.The Journal of biological chemistry · 2025Article
- Inhibition of BET proteins modulates amyloid-beta accumulation and cognitive performance in middle-aged mice prenatally exposed to maternal immune activation.Frontiers in molecular neuroscience · 2025Article
- Rational fusion design inspired by cell-penetrating peptide: SS31/S-14 G Humanin hybrid peptide with amplified multimodal efficacy and bio-permeability for the treatment of Alzheimer's disease.Asian journal of pharmaceutical sciences · 2024Article
- Review
- Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.Aging and disease · 2024Review
- Long term worsening of amyloid pathology, cerebral function, and cognition after a single inoculation of beta-amyloid seeds with Osaka mutation.Acta neuropathologica communications · 2023Article
- Aβ42 oligomer-specific antibody ALZ-201 reduces the neurotoxicity of Alzheimer's disease brain extracts.Alzheimer's research & therapy · 2022Article
- Neurexin-β Mediates the Synaptogenic Activity of Amyloid Precursor Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Evaluation of Synaptic and Axonal Dysfunction Biomarkers in Alzheimer's Disease and Mild Cognitive Impairment Based on CSF and Bioinformatic Analysis.International journal of molecular sciences · 2022Article
- A novel non‑selective atypical PKC agonist could protect neuronal cell line from Aβ‑oligomer induced toxicity by suppressing Aβ generation.Molecular medicine reports · 2022Article
- The plasminogen activating system in the pathogenesis of Alzheimer's disease.Neural regeneration research · 2021Review
- Insulin Resistance Exacerbates Alzheimer Disease via Multiple Mechanisms.Frontiers in neuroscience · 2021Review
- Review
- Anti-inflammatory and memory-enhancing properties of Chinese herbal extracts: The possible application in Alzheimer's disease.Tzu chi medical journalReview
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations of excitatory synaptic function are the strongest correlate to the pathologic disturbance of cognitive ability observed in the early stages of Alzheimer's disease (AD). This pathologic feature is driven by amyloid-β oligomers (Aβos) and propagates from neuron to neuron. Here, we investigated the mechanism by which Aβos affect the function of synapses and how these alterations propagate to surrounding healthy neurons. We used complementary techniques ranging from electrophysiological recordings and molecular biology to confocal microscopy in primary cortical cultures, and from acute hippocampal and cortical slices from male wild-type and amyloid precursor protein (APP) knock-out (KO) mice to assess the effects of Aβos on glutamatergic transmission, synaptic plasticity, and dendritic spine structure. We showed that extracellular application of Aβos reduced glutamatergic synaptic transmission and long-term potentiation. These alterations were not observed in APP KO neurons, suggesting that APP expression is required. We demonstrated that Aβos/APP interaction increases the amyloidogenic processing of APP leading to intracellular accumulation of newly produced Aβos. Intracellular Aβos participate in synaptic dysfunctions as shown by pharmacological inhibition of APP processing or by intraneuronal infusion of an antibody raised against Aβos. Furthermore, we provide evidence that following APP processing, extracellular release of Aβos mediates the propagation of the synaptic pathology characterized by a decreased spine density of neighboring healthy neurons in an APP-dependent manner. Together, our data unveil a complementary role for Aβos in AD, while intracellular Aβos alter synaptic function, extracellular Aβos promote a vicious cycle that propagates synaptic pathology from diseased to healthy neurons.
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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.