GFAP and Astrogliosis
Open accessAbstract
One of the most remarkable characteristics of astrocytes is their vigorous response to diverse neurologic insults, a feature that is well conserved across a variety of different species. The astroglial response occurs rapidly and can be detected within one hour of a focal mechanical trauma (Mucke et al., 1991). Prominent reactive astrogliosis is seen; in AIDS dementia; a variety of other viral infections; prion associated spongiform encephalopathies; inflammatory demyelinating diseases; acute traumatic brain injury; neurodegenerative diseases such as Alzheimer's disease. The prominence of astroglial reactions in various diseases, the rapidity of the astroglial response and the evolutionary conservation of reactive astrogliosis indicate that reactive astrocytes fulfill important functions of the central nervous system (CNS). Yet, the exact role reactive astrocytes play in the injured CNS has so far remained elusive. This chapter summaries the various experimental models and diseases that exhibit astrogliosis and increase in glial fibrillary acidic protein (GFAP). Recent in vitro studies to inhibit GFAP synthesis are also presented.
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Early astrocyte changes included upregulation of cellular adhesion molecules, neuronal guidance cues, signaling receptors, and GFAP.
“Early changes included upregulation of cellular adhesion molecules (CADM1, CDRH3, PCDHGA1, PCDHB14, PCDHB16, CLSTN1, ITGA6, NEO1, ANOS1) and neuronal guidance cues (NLGN3, NTRK3, SEMA4B, NTNG2), signaling receptors (PTCHD1, NRP1, BMPR2, UNC5C)70 and GFAP, a known hallmark of AD and astrogliosis71 (Fig. 6j, top).”
From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [71]
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- Authors
- Eng, L. F., & Ghirnikar, R. S.
- Affiliations
- United States Department of Veterans Affairs (US)
- Stanford Medicine (US)
- Corresponding author
- Eng, Lawrence F.
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 1994-07
- Volume
- 4
- Issue
- 3
- Pages
- 229-237
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- OpenAlex
- W1971213127
- Cited by
- 864
- References
- 2
- Citations by year
- 2026: 15 · 2025: 28 · 2024: 29 · 2023: 20 · 2022: 46 · 2021: 37 · 2020: 34 · 2019: 27 · 2018: 26 · 2017: 31 · 2016: 30 · 2015: 29 · 2014: 31 · 2013: 44 · 2012: 31
- FWCI
- 2.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain Pathology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- National Institutes of Health (5r01ns011632-22)
- National Institute of Neurological Disorders and Stroke (NS-11632)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- glial fibrillary acidic protein, reactive astrogliosis, astrocytes, neuroinflammation, traumatic brain injury, HIV-associated dementia, viral encephalitis, demyelinating disease, Alzheimer's disease, neurodegenerative diseases, central nervous system injury
- MeSH terms
- Animals, Astrocytes, Brain, Brain Diseases, Brain Neoplasms, Cells, Cultured, Glial Fibrillary Acidic Protein, Glioma, Humans, Immunohistochemistry, Species Specificity, Biomarkers
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