Astrocytes are important mediators of Aβ-induced neurotoxicity and tau phosphorylation in primary culture
Open accessAbstract
Alzheimer's disease (AD) is pathologically characterised by the age-dependent deposition of β-amyloid (Aβ) in senile plaques, intraneuronal accumulation of tau as neurofibrillary tangles, synaptic dysfunction and neuronal death. Neuroinflammation, typified by the accumulation of activated microglia and reactive astrocytes, is believed to modulate the development and/or progression of AD. We have used primary rat neuronal, astrocytic and mixed cortical cultures to investigate the contribution of astrocyte-mediated inflammatory responses during Aβ-induced neuronal loss. We report that the presence of small numbers of astrocytes exacerbate Aβ-induced neuronal death, caspase-3 activation and the production of caspase-3-cleaved tau. Furthermore, we show that astrocytes are essential for the Aβ-induced tau phosphorylation observed in primary neurons. The release of soluble inflammatory factor(s) from astrocytes accompanies these events, and inhibition of astrocyte activation with the anti-inflammatory agent, minocycline, reduces astrocytic inflammatory responses and the associated neuronal loss. Aβ-induced increases in caspase-3 activation and the production of caspase-3-truncated tau species in neurons were reduced when the astrocytic response was attenuated with minocycline. Taken together, these results show that astrocytes are important mediators of the neurotoxic events downstream of elevated Aβ in models of AD, and suggest that mechanisms underlying pro-inflammatory cytokine release might be an important target for therapy.
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Astrocytes become activated in AD and exhibit certain immune functions.
“Astrocytes become activated in AD and exhibit certain immune functions.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [96]
Astrocytes exacerbate Aβ-induced tau hyperphosphorylation and truncation.
“Astrocytes exacerbate Aβ-induced tau hyperphosphorylation and truncation.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [96]
The results are consistent with literature indicating that different types of glia may contribute to Alzheimer's disease via different regulatory mechanisms.
“These results are consistent with a newly emerging literature which indicates that different types of glia may contribute to the disease via different regulatory mechanisms55–57.”
From Neuronal and glial 3D chromatin architecture informs the cellular etiology of brain disorders (2021) · cites this paper as [55]
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- Authors
- Garwood, C. J., Pooler, A. M., Atherton, J., Hanger, D. P., & Noble, W.
- Affiliations
- King's College London (GB)
- Corresponding author
- Noble, W
- Venue
- Cell Death & Disease
- Published
- 2011-06-02
- Volume
- 2
- Issue
- 6
- Pages
- e167-e167
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC3168992
- OpenAlex
- W2017666196
- Cited by
- 379
- References
- 42
- Citations by year
- 2026: 18 · 2025: 30 · 2024: 26 · 2023: 20 · 2022: 28 · 2021: 47 · 2020: 42 · 2019: 12 · 2018: 25 · 2017: 29 · 2016: 24 · 2015: 16 · 2014: 23 · 2013: 18 · 2012: 19
- FWCI
- 13.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (unspecified)
- Locations
- Cell Death and Disease (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Wellcome Trust
- Alzheimer's Society
- Henry Smith Charity
- Medical Research Council
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- astrocytes, amyloid-beta, Alzheimer's disease, neuroinflammation, tau phosphorylation, caspase-3, neuronal cell death, minocycline, inflammatory cytokines, astrocyte activation, neurofibrillary tangles, amyloid plaques
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Neurons, Peptide Fragments, Phosphorylation, Amyloid beta-Peptides, tau Proteins, Cell Death, Rats
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