ArticleScientific reports2017
Amyloid-β Oligomers Interact with Neurexin and Diminish Neurexin-mediated Excitatory Presynaptic Organization.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Article
- DeepPlaque: a scalable multimodal platform for Aβ pathology and cell analysis in Alzheimer's disease.EMBO molecular medicine · 2026Article
- Retinal proteome changes mirror brain pathology and reveal synaptic and cytoskeletal dysfunction in Alzheimer's disease.Acta neuropathologica · 2026Article
- Neurexins, Ephrin receptors, and N-cadherin signaling as emerging mechanisms in synaptic dysfunction and neurodegenerative diseases.Communications biology · 2026Review
- The Neurexin1β Histidine-Rich Domain Is Involved in Excitatory Presynaptic Organization and Short-Term Plasticity.eNeuro · 2026Article
- Transsynaptic complex dysfunction in the hippocampus of Alzheimer's disease patients.Frontiers in aging neuroscience · 2026Article
- Deletion of neuronal Idol ameliorates Alzheimer's disease-related pathologies via APOE receptors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A Peptide Motif Covering Splice Site B in Neuroligin-1 Binds to Aβ and Acts as a Neprilysin Inhibitor.Molecular neurobiology · 2025Article
- Functional Connectivity Favors Aberrant Visual Network c-Fos Expression Accompanied by Cortical Synapse Loss in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Article
- Role of Neurexins in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- α-Synuclein Preformed Fibrils Bind to β-Neurexins and Impair β-Neurexin-Mediated Presynaptic Organization.Cells · 2023Article
- SorCS1 inhibits amyloid-β binding to neurexin and rescues amyloid-β-induced synaptic pathology.Life science alliance · 2023Article
- A novel rhein-huprine hybrid ameliorates disease-modifying properties in preclinical mice model of Alzheimer's disease exacerbated with high fat diet.Cell & bioscience · 2023Article
- Neurexin-β Mediates the Synaptogenic Activity of Amyloid Precursor Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Synaptogenic effect ofScience translational medicine · 2022Article
- 7,8-Dihydroxycoumarin Alleviates Synaptic Loss by Activated PI3K-Akt-CREB-BDNF Signaling in Alzheimer's Disease Model Mice.Journal of agricultural and food chemistry · 2022Article
- 1-(7-Chloroquinolin-4-yl)-N-(4-Methoxybenzyl)-5-Methyl-1H-1,2, 3-Triazole-4- carboxamide Reduces Aβ Formation and Tau Phosphorylation in Cellular Models of Alzheimer's Disease.Neurochemical research · 2022Article
- Neuronal Cell Adhesion Molecules May Mediate Neuroinflammation in Autism Spectrum Disorder.Frontiers in psychiatry · 2022Review
- Amyloid precursor protein (APP) and amyloid β (Aβ) interact with cell adhesion molecules: Implications in Alzheimer's disease and normal physiology.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by excessive production and deposition of amyloid-beta (Aβ) proteins as well as synapse dysfunction and loss. While soluble Aβ oligomers (AβOs) have deleterious effects on synapse function and reduce synapse number, the underlying molecular mechanisms are not well understood. Here we screened synaptic organizer proteins for cell-surface interaction with AβOs and identified a novel interaction between neurexins (NRXs) and AβOs. AβOs bind to NRXs via the N-terminal histidine-rich domain (HRD) of β-NRX1/2/3 and alternatively-spliced inserts at splicing site 4 of NRX1/2. In artificial synapse-formation assays, AβOs diminish excitatory presynaptic differentiation induced by NRX-interacting proteins including neuroligin1/2 (NLG1/2) and the leucine-rich repeat transmembrane protein LRRTM2. Although AβOs do not interfere with the binding of NRX1β to NLG1 or LRRTM2, time-lapse imaging revealed that AβO treatment reduces surface expression of NRX1β on axons and that this reduction depends on the NRX1β HRD. In transgenic mice expressing mutated human amyloid precursor protein, synaptic expression of β-NRXs, but not α-NRXs, decreases. Thus our data indicate that AβOs interact with NRXs and that this interaction inhibits NRX-mediated presynaptic differentiation by reducing surface expression of axonal β-NRXs, providing molecular and mechanistic insights into how AβOs lead to synaptic pathology in AD.
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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.