Role of GFAP in CNS injuries

Brenner, Michael

doi:10.1016/j.neulet.2014.01.055

Cited by 222Traumatic Brain Injury and Neurovascular DisturbancesBarrier Structure and Function StudiesNeuroinflammation and Neurodegeneration Mechanisms

Role of GFAP in CNS injuries

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Brenner, Michael·2014·Neuroscience Letters

DOI 10.1016/j.neulet.2014.01.055PMC PMC4049287

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Abstract

The role of GFAP in CNS injury is reviewed as revealed by studies using GFAP null mice. In order to provide background information for these studies, the effects of absence of GFAP in the uninjured astrocyte are also described. Activities attributable to GFAP include suppressing neuronal proliferation and neurite extension in the mature brain, forming a physical barrier to isolate damaged tissue, regulating blood flow following ischemia, contributing to the blood-brain barrier, supporting myelination, and providing mechanical strength. However, findings for many of these roles have been variable among laboratories, pointing to the presence of unappreciated complexity in GFAP function. One complexity may be regional differences in GFAP activities; others are yet to be discovered.

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GFAP is a marker for astrocytic activation and gliosis, with its production upregulated.
“The highly brain-specific protein GFAP has been studied as a potential marker for astrocytic activation and gliosis, upon which its production is being upregulated [29, 30].”
From A Combination of Neurofilament Light, Glial Fibrillary Acidic Protein, and Neuronal Pentraxin-2 Discriminates Between Frontotemporal Dementia and Other Dementias (2022) · cites this paper as [29]
Chronic activation of glial cells may directly lead to deterioration of the underlying disease pathology by the accumulation of cytotoxic factors.
“A chronic activation of these cells may directly lead to a deterioration of the underlying disease pathology by the accumulation of cytotoxic factors [29, 85].”
From A Combination of Neurofilament Light, Glial Fibrillary Acidic Protein, and Neuronal Pentraxin-2 Discriminates Between Frontotemporal Dementia and Other Dementias (2022) · cites this paper as [29]

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Authors: Brenner, M.
Affiliations: Civitan International (US)
Corresponding author: Brenner, Michael
Venue: Neuroscience Letters
Publisher: Elsevier BV
Published: 2014-04
Volume: 565
Pages: 7-13
ISSN: 0304-3940 (ISSN-L)
DOI: 10.1016/j.neulet.2014.01.055
PMC: PMC4049287
OpenAlex: W2063042123
Cited by: 222
References: 51
Citations by year: 2026: 13 · 2025: 25 · 2024: 26 · 2023: 20 · 2022: 25 · 2021: 34 · 2020: 24 · 2019: 19 · 2018: 7 · 2017: 8 · 2016: 5 · 2015: 10 · 2014: 6
FWCI: 1.32
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience Letters (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: NINDS (RO1NS39055, P01NS42803)
Topics: Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: glial fibrillary acidic protein, central nervous system injury, astrocytes, neuronal proliferation, neurite outgrowth, blood-brain barrier, ischemia, myelination, mechanical support
MeSH terms: Animals, Astrocytes, Blood-Brain Barrier, Brain Injuries, Cell Adhesion, Brain Ischemia, Glial Fibrillary Acidic Protein, Myelin Sheath, Nerve Tissue Proteins, Neurons, Vimentin, Long-Term Potentiation, Mice, Knockout, Long-Term Synaptic Depression, Cell Proliferation

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Role of GFAP in CNS injuries

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