Deciphering the astrocyte reaction in Alzheimer's disease
Open accessAbstract
amyloid plaques in the cortex of Alzheimer's disease (AD) patients several decades ago. However, their role in AD pathophysiology has remained elusive ever since, in part owing to the extrapolation of the literature from primary astrocyte cultures and acute brain injury models to a chronic neurodegenerative scenario. Recent accumulating evidence supports the idea that reactive astrocytes in AD acquire neurotoxic properties, likely due to both a gain of toxic function and a loss of their neurotrophic effects. However, the diversity and complexity of this glial cell is only beginning to be unveiled, anticipating that astrocyte reaction might be heterogeneous as well. Herein we review the evidence from mouse models of AD and human neuropathological studies and attempt to decipher the main conundrums that astrocytes pose to our understanding of AD development and progression. We discuss the morphological features that characterize astrocyte reaction in the AD brain, the consequences of astrocyte reaction for both astrocyte biology and AD pathological hallmarks, and the molecular pathways that have been implicated in this reaction.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Mouse hippocampal astrocytes showed increased GFAP immunofluorescence intensity.
“Similarly, mouse hippocampal astrocytes also showed increased GFAP immunofluorescence intensity, commonly considered a direct measure of astrocyte reactivity [90].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [90]
The ‘Proliferation or Just Phenotypic Change?’ section describes enhanced GFAP immunoreactivity in the AD brain and says reactive astrocytes are conventionally identified by it. It reports similar numbers of GFAP-positive astrocytes in wild-type and 3xTg AD mouse hippocampi, but does not report increased GFAP immunofluorescence intensity in those mice; similar cell counts do not establish fluorescence intensity. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAstrocyte morphology changes near Aβ plaques and pTau NFTs.
“Because astrocyte morphology changes near Aβ plaques and pTau NFTs23,24”
From Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease (2024) · cites this paper as [24]
The role of reactive astrocytes remains unclear in terms of plaque formation, Aβ clearance and plaque growth restriction.
“The role of reactive astrocytes remains unclear in terms of plaque formation, Aβ clearance and plaque growth restriction [50,51].”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 231 · Cited by 282
- Authors
- Perez-Nievas, B. G., & Serrano-Pozo, A.
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-04-25
- Volume
- 10
- Pages
- 114-114
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC5996928
- OpenAlex
- W2801244110
- Cited by
- 282
- References
- 231
- Citations by year
- 2026: 22 · 2025: 28 · 2024: 28 · 2023: 39 · 2022: 42 · 2021: 60 · 2020: 43 · 2019: 18 · 2018: 1
- FWCI
- 4.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- Alzheimer’s Research UK (ARUK-RF2014-2)
- National Institute of Neurological Disorders and Stroke (R25NS065743)
- Alzheimer’s Association (AACF-17-524184)
- 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
- Alzheimer's disease, reactive astrocytes, amyloid plaques, neurotoxicity, astrocyte heterogeneity, astrocyte morphology, molecular pathways, mouse models of Alzheimer's disease, neuropathology
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
