ArticleASN neuro2010
Amyloid β-peptide directly induces spontaneous calcium transients, delayed intercellular calcium waves and gliosis in rat cortical astrocytes.
Article in ASN neuro, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Role of dysregulated calcium homeostasis in astrocytes in neurodegenerative disorders.Nature reviews. Neuroscience · 2026Review
- Neurotoxic amyloid β-peptide and tau produce cytokine-like effects on PMCA in glioblastoma cell lines, enhancing its activity and isoforms expression.FEBS open bio · 2025Article
- Amyloid-β-induced alteration of fast and localized calcium elevations in cultured astrocytes.Scientific reports · 2025Article
- Lysosomal acidification impairment in astrocyte-mediated neuroinflammation.Journal of neuroinflammation · 2025Review
- mGluR5 as a Potential Orchestrator of Astrocyte Interactions in Neurological Disorders.Neural plasticity · 2025Review
- ACognitive neurodynamics · 2024Article
- An Immune-Independent Mode of Action of Tacrolimus in Promoting Human Extravillous Trophoblast Migration Involves Intracellular Calcium Release and F-Actin Cytoskeletal Reorganization.International journal of molecular sciences · 2024Article
- Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2024Review
- Unlocking the therapeutic potential of P2X7 receptor: a comprehensive review of its role in neurodegenerative disorders.Frontiers in pharmacology · 2024Review
- Astrocyte adaptation in Alzheimer's disease: a focus on astrocytic P2X7R.Essays in biochemistry · 2023Review
- AβCellular and molecular life sciences : CMLS · 2022Article
- Article
- Astrocytes respond to a neurotoxic Aβ fragment with state-dependent CaActa neuropathologica communications · 2021Article
- Astroglial Calcium Signaling in Aging and Alzheimer's Disease.Cold Spring Harbor perspectives in biology · 2019Review
- Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade.Molecular neurodegeneration · 2019Article
- Astroglia in Alzheimer's Disease.Advances in experimental medicine and biology · 2019Review
- S100 Proteins in Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- CaJournal of neuroinflammation · 2018Article
- Astrocytic Pathological Calcium Homeostasis and Impaired Vesicle Trafficking in Neurodegeneration.International journal of molecular sciences · 2017Review
- Amyloid-β and Astrocytes Interplay in Amyloid-β Related Disorders.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The contribution of astrocytes to the pathophysiology of AD (Alzheimer's disease) and the molecular and signalling mechanisms that potentially underlie them are still very poorly understood. However, there is mounting evidence that calcium dysregulation in astrocytes may be playing a key role. Intercellular calcium waves in astrocyte networks in vitro can be mechanically induced after Aβ (amyloid β-peptide) treatment, and spontaneously forming intercellular calcium waves have recently been shown in vivo in an APP (amyloid precursor protein)/PS1 (presenilin 1) Alzheimer's transgenic mouse model. However, spontaneous intercellular calcium transients and waves have not been observed in vitro in isolated astrocyte cultures in response to direct Aβ stimulation in the absence of potentially confounding signalling from other cell types. Here, we show that Aβ alone at relatively low concentrations is directly able to induce intracellular calcium transients and spontaneous intercellular calcium waves in isolated astrocytes in purified cultures, raising the possibility of a potential direct effect of Aβ exposure on astrocytes in vivo in the Alzheimer's brain. Waves did not occur immediately after Aβ treatment, but were delayed by many minutes before spontaneously forming, suggesting that intracellular signalling mechanisms required sufficient time to activate before intercellular effects at the network level become evident. Furthermore, the dynamics of intercellular calcium waves were heterogeneous, with distinct radial or longitudinal propagation orientations. Lastly, we also show that changes in the expression levels of the intermediate filament proteins GFAP (glial fibrillary acidic protein) and S100B are affected by Aβ-induced calcium changes differently, with GFAP being more dependent on calcium levels than S100B.
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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.