ArticleIn vitro cellular & developmental biology. Animal2011
The effects of amyloid-β42 oligomer on the proliferation and activation of astrocytes in vitro.
Article in In vitro cellular & developmental biology. Animal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
The trial behind it
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Who cites it
31 citing papers in PubMed.
- Amyloid beta pathology induces astrocytic pTDP-43 mislocalization and disrupts TDP-43-regulated cryptic exon transcripts.Frontiers in aging neuroscience · 2026Article
- Stage-Dependent Function of Astrocytes in Alzheimer's Disease: A Review.Neuroscience insights · 2026Review
- Modulation of AβActa biochimica et biophysica Sinica · 2025Article
- Amelioration of Astrocytic Dysfunction via AQP4/LRP1 Pathway byJournal of microbiology and biotechnology · 2025Article
- Research Progress on the Pathogenesis, Diagnosis, and Drug Therapy of Alzheimer's Disease.Brain sciences · 2024Review
- Polar lipids modify Alzheimer's Disease pathology by reducing astrocyte pro-inflammatory signaling through platelet-activating factor receptor (PTAFR) modulation.Lipids in health and disease · 2024Article
- The AβFrontiers in cellular neuroscience · 2024Article
- Measures of cortical microstructure are linked to amyloid pathology in Alzheimer's disease.Brain : a journal of neurology · 2023Article
- The Eye as a Diagnostic Tool for Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Amyloid-β in Alzheimer's disease - front and centre after all?Neuronal signaling · 2023Review
- 5-Methyltetrahydrofolate Alleviates Memory Impairment in a Rat Model of Alzheimer's Disease Induced by D-Galactose and Aluminum Chloride.International journal of environmental research and public health · 2022Article
- Ex vivo expanded human regulatory T cells modify neuroinflammation in a preclinical model of Alzheimer's disease.Acta neuropathologica communications · 2022Article
- The role of astrocytes in prion-like mechanisms of neurodegeneration.Brain : a journal of neurology · 2022Review
- Neuronal Glial Crosstalk: Specific and Shared Mechanisms in Alzheimer's Disease.Brain sciences · 2022Review
- A Neuron, Microglia, and Astrocyte Triple Co-culture Model to Study Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- Alzheimer's Disease Progressively Reduces Visual Functional Network Connectivity.Journal of Alzheimer's disease reports · 2021Article
- The physiology of regulated BDNF release.Cell and tissue research · 2020Review
- Human iPSC-derived Down syndrome astrocytes display genome-wide perturbations in gene expression, an altered adhesion profile, and increased cellular dynamics.Human molecular genetics · 2020Article
- Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβInternational journal of medical sciences · 2020Article
- Astrocyte activation and altered metabolism in normal aging, age-related CNS diseases, and HAND.Journal of neurovirology · 2019Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies reported that astrocyte response to amyloid-β (Aβ) before obvious neuronal damage could be detected in Alzheimer's disease (AD). It is suggested that astrocytes play a key role in AD pathologies. In this study, we investigated the effects of Aβ(42) oligomer on the proliferation and activation of astrocytes by in vitro experiments. The results showed that Aβ(42) oligomers could convert astrocytes to responsive astrocytes. It was revealed by MTT and ELISA assays that the viability of astrocytes gradually decreased, and the release of brain-derived neurotrophic factor increased with elevated Aβ(42) concentration and prolonged duration. Reverse-transcription polymerase chain reaction (RT-PCR) assay indicated that Aβ(42) oligomers increased the expression of glial fibers acid protein and interleukin-1β in a dose-dependent but not time-dependent manner. It was showed that A8, a mouse monoclonal antibody, was able to protect the cultured astrocytes against the toxicity of Aβ(42) oligomers. The result demonstrated that A8 could inhibit Aβ(42) oligomers toxic effects on astrocytes and that, alone, A8 could promote the proliferation of astrocytes in certain time. The present study laid a theoretical foundation for further understanding the effects of Aβ(42) on astrocytes and, hence, is conducive to the theoretical understanding and clinical therapies of AD progression.
Indexed as
Identifiers
21858610What OpenQuestion holds
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.