ArticleScientific reports2018
The contribution of microglia to early synaptic compensatory responses that precede β-amyloid-induced neuronal death.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Retinitis pigmentosa elicits neurodegeneration within the visual pathway in REEP6 knockout mice.Neural regeneration research · 2026Article
- Tunable acoustic rotation for deep biophysical phenotyping of preclinical Alzheimer's disease.Materials today. Bio · 2026Article
- Microglial Activation Under Hypoxic Conditions in Early Alzheimer's Disease: Can Natural SIRT1 Activators Be Therapeutic Allies in the Inflammation-Energy Axis?Phytotherapy research : PTR · 2026Review
- Chemically Selective Nanoelectrode Arrays for Real-Time, Parallel Neurotransmitter and Electrical Recording.Small science · 2026Article
- Hypoxia reverses the early anti-inflammatory microglial response to the β-amyloid peptide: mitochondrial involvement and beneficial roles of melatonin and naringenin.Journal of translational medicine · 2025Article
- The interaction of BDNF with estrogen in the development of hypertension and obesity, particularly during menopause.Frontiers in endocrinology · 2024Review
- Synapse Regulation.Advances in neurobiology · 2024Review
- Melatonin Activates Anti-Inflammatory Features in Microglia in a Multicellular Context: Evidence from Organotypic Brain Slices and HMC3 Cells.Biomolecules · 2023Article
- Microglia and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release.International journal of molecular sciences · 2022Article
- Review
- Proficiency of Extracellular Vesicles From hiPSC-Derived Neural Stem Cells in Modulating Proinflammatory Human Microglia: Role of Pentraxin-3 and miRNA-21-5p.Frontiers in molecular neuroscience · 2022Article
- SIRT1-Dependent Upregulation of BDNF in Human Microglia Challenged with Aβ: An Early but Transient Response Rescued by Melatonin.Biomedicines · 2021Article
- The physiology of regulated BDNF release.Cell and tissue research · 2020Review
- POSCAbilities: The Application of the Prion Organotypic Slice Culture Assay to Neurodegenerative Disease Research.Biomolecules · 2020Review
- SIRT1 Mediates Melatonin's Effects on Microglial Activation in Hypoxia: In Vitro and In Vivo Evidence.Biomolecules · 2020Article
- Reciprocal Interplay Between Astrocytes and CD4+ Cells Affects Blood-Brain Barrier and Neuronal Function in Response to β Amyloid.Frontiers in molecular neuroscience · 2020Article
- The Ambiguous Role of Microglia in Aβ Toxicity: Chances for Therapeutic Intervention.Current neuropharmacology · 2020Review
- Carnosine Prevents Aβ-Induced Oxidative Stress and Inflammation in Microglial Cells: A Key Role of TGF-β1.Cells · 2019Article
- Astrocytes Modify Migration of PBMCs Induced by β-Amyloid in a Blood-Brain BarrierFrontiers in cellular neuroscience · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glial-neuronal cross-talk has a critical role in the development of neurodegenerative conditions, including Alzheimer's Disease, where it affects neuronal responses to β-amyloid peptide (Aβ)-induced toxicity. We set out to identify factors regulating synaptic responses to Aβ, dissecting the specific role of glial signaling. A low concentration of aggregated Aβ42 induced selective up-regulation of mature brain-derived neurotrophic factor (BDNF) expression and release in rat organotypic hippocampal cultures as well as in cortical pure microglia. Conditioned media from resting (CMC) or Aβ42-treated (CMA) microglia were tested for their effects on synaptophysin expression in SH-SY5Y neuronal-like cells during challenge with Aβ42. Both CMC and CMA prevented Aβ-induced synaptophysin loss. In the presence of Aβ + CMA, synaptophysin was over-expressed, although it appeared partly clumped in cell bodies. Synaptophysin over-expression was not directly dependent on BDNF signaling on neuronal-like cells, but relied on autocrine BDNF action on microglia. FM1-43 labeling experiments revealed compromised synaptic vesicle recycling in Aβ42-treated neuronal-like cells, rescued by microglial conditioned medium. In these conditions, significant and prolonged neuroprotection was observed. Our results point to microglia as a target for early intervention, given its positive role in supporting neuronal compensatory responses to Aβ synaptotoxicity, which potentially lead to their extended survival.
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