When astrocytes become harmful: Functional and inflammatory responses that contribute to Alzheimer's disease
Abstract
A growing body of research suggests that astrocytes play roles as contributors to the pathophysiology of Alzheimer's disease (AD). Several lines of evidence propose that activated astrocytes produce and release proinflammatory molecules that may be critical for the generation of amyloid-β peptide (Aβ). However, accumulating evidence indicates that Aβ may activate astrocytes, which leads to an increase in cytokines that has been suggested to be a causative factor in the cognitive dysfunction of AD; thus, a vicious circle may be created. Intrinsic inflammatory mechanisms may provide a regulatory system that is capable of influencing the neuronal microenvironment that affects neuronal survival. In this article, we address the evidence surrounding the interactions of dysfunctional astrocytes with neighboring neurons that may initiate a cascade of events that culminates with neuronal injury and the expression of the hallmark lesions of AD. Comprehensive knowledge of the molecular mechanisms underlying the participation of astrocytes in neurodegeneration could aid the development of therapies to restore proper astrocyte function that can be used in AD patients to prevent or alleviate the progression of the disease in a more efficient and comprehensive manner.
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Reactive astrocytes contribute to neuroinflammatory processes associated with AD pathology.
“Recent evidence suggests that reactive astrocytes also contribute to neuroinflammatory processes associated with AD pathology [93].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [93]
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- Authors
- Avila-Muñoz, E., & Arias, C.
- Affiliations
- Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (MX)
- Corresponding author
- Arias, Clorinda
- ORCID
- Arias, Clorinda
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 18
- Pages
- 29-40
- ISSN
- 1568-1637 (ISSN-L)
- OpenAlex
- W2017431945
- Cited by
- 114
- References
- 211
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 3 · 2023: 7 · 2022: 3 · 2021: 13 · 2020: 10 · 2019: 6 · 2018: 10 · 2017: 8 · 2016: 19 · 2015: 20 · 2014: 2
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Ageing Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- CONACYT (166482, 239696)
- 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, Alzheimer's disease, neuroinflammation, amyloid-beta, cytokines, astrocyte-neuron interaction, neurodegeneration, cognitive impairment, neuronal injury, astrocyte dysfunction
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Humans, Inflammation, Neurons, Signal Transduction, Amyloid beta-Peptides, Inflammation Mediators, Paracrine Communication
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 ›
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