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Review: Astrocytes in Alzheimer's disease and other age‐associated dementias: a supporting player with a central role
Abstract
Astrocytes have essential roles in the central nervous system and are also implicated in the pathogenesis of neurodegenerative disease. Forming non‐overlapping domains, astrocytes are highly complex cells. Immunohistochemistry to a variety of proteins can be used to study astrocytes in tissue, labelling different cellular components and sub‐populations, including glial fibrillary acidic protein, ALDH 1L1, CD 44, NDRG 2 and amino acid transporters, but none of these labels the entire astrocyte population. Increasing heterogeneity is recognized in the astrocyte population, a complexity that is relevant both to their normal function and pathogenic roles. They are involved in neuronal support, as active components of the tripartite synapse and in cell interactions within the neurovascular unit (NVU), where they are essential for blood–brain barrier maintenance and neurovascular coupling. Astrocytes change with age, and their responses may modulate the cellular effects of neurodegenerative pathologies, which alone do not explain all of the variance in statistical models of neurodegenerative dementias. Astrocytes respond to both the neurofibrillary tangles and plaques of Alzheimer's disease, to hyperphosphorylated tau and Aβ, eliciting an effect which may be neuroprotective or deleterious. Not only astrocyte hypertrophy, in the form of gliosis, occurs, but also astrocyte injury and atrophy. Loss of normal astrocyte functions may contribute to reduced support for neurones and dysfunction of the NVU. Understanding how astrocytes contribute to dementia requires an understanding of the underlying heterogeneity of astrocyte populations, and the complexity of their responses to pathology. Enhancing the supportive and neuroprotective components of the astrocyte response has potential translational applications in therapeutic approaches to dementia.
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“For instance, when astrocytes become senescent they no longer provide trophic support to the neuron, disturbing normal neuronal function [43].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [43]
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Metadata
- Authors
- Garwood, C. J., Ratcliffe, L. E., Simpson, J. E., Heath, P. R., Ince, P. G., & Wharton, S. B.
- Affiliations
- University of Sheffield (GB)
- Corresponding author
- Garwood, C. J.
- Venue
- Neuropathology and Applied Neurobiology
- Publisher
- Wiley
- Published
- 2017-05-22
- Volume
- 43
- Issue
- 4
- Pages
- 281-298
- ISSN
- 0305-1846 (ISSN-L)
- 1365-2990
- OpenAlex
- W2497919201
- Cited by
- 233
- References
- 155
- Citations by year
- 2026: 10 · 2025: 20 · 2024: 26 · 2023: 21 · 2022: 26 · 2021: 43 · 2020: 23 · 2019: 22 · 2018: 21 · 2017: 20
- FWCI
- 2.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropathology and Applied Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- Funders
- Alzheimer Society
- Alzheimer’s Research UK (ART PG2006/6, ART PG2010‐5)
- Biotechnology and Biological Sciences Research Council (BB/K006711/1)
- Medical Research Council (MRC/J004308/1, MRC/G9901400)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, astrocyte heterogeneity, neurovascular unit, blood-brain barrier, neurovascular coupling, tripartite synapse, gliosis, astrocyte injury, neurofibrillary tangles, amyloid plaques, hyperphosphorylated tau, amyloid-beta, astrocyte subpopulations, neuroprotection
- MeSH terms
- Aging, Alzheimer Disease, Animals, Astrocytes, Dementia, Humans
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