Alexander Disease
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### Introduction The past decade has witnessed a burst of speculation and data about how astrocyte dysfunction contributes to the phenotypes of the well known neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and amyotrophic lateral sclerosis, as well as other types of
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Astrocytes can exhibit cell-autonomous disturbances, as in astrocytopathies caused by mutated astrocytic genes such as GFAP in Alexander disease, direct viral infections, or toxic substances that specifically damage astrocytes such as ammonium in hepatic encephalopathy.
“Astrocytes may also exhibit cell-autonomous disturbances8, as happens in astrocytopathies resulting from mutated alleles of astrocytic genes (for example, GFAP in Alexander disease)9, as well as from direct viral infections or exposure to toxic substances that specifically damage astrocytes (for example, ammonium in hepatic encephalopathy)10.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [9]
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- Tian R Wu X Hagemann TL Sosunov AA Messing A McKhann GM Goldman JE Alexander disease mutant GFAP compromises glutamate transport in astrocytes J Neuropathol Exp Neurol 2010 69 335 345 20448479 PMC3342699
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Astrocyte pathology in Alexander disease causes a marked inflammatory environment
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General Pathophysiology of Astroglia
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Disorders of Astrocytes: Alexander Disease as a Model
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Nitric oxide mediates glial-induced neurodegeneration in Alexander disease
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Tissue and cellular rigidity and mechanosensitive signaling activation in Alexander disease
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The role of gigaxonin in the degradation of the glial-specific intermediate filament protein GFAP
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Further delineation of the phenotypic spectrum of ISCA2 defect: A report of ten new cases
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Refining the concept of GFAP toxicity in Alexander disease
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- Authors
- Messing, A., Brenner, M., Feany, M. B., Nedergaard, M., & Goldman, J. E.
- Affiliations
- University of Wisconsin–Madison (US)
- University of Alabama at Birmingham (US)
- University of Rochester Medicine (US)
- Columbia University (US)
- Corresponding author
- Messing, Albee
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-04-11
- Volume
- 32
- Issue
- 15
- Pages
- 5017-5023
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3336214
- OpenAlex
- W4251359871
- Cited by
- 250
- References
- 55
- Citations by year
- 2026: 14 · 2025: 18 · 2024: 21 · 2023: 17 · 2022: 17 · 2021: 21 · 2020: 11 · 2019: 17 · 2018: 18 · 2017: 15 · 2016: 24 · 2015: 19 · 2014: 19 · 2013: 17 · 2012: 1
- FWCI
- 9.02
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS060120, NS-42803, NS 22475, R01NS022475, P01NS042803, NS-060120)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 03352, P01HD076892, R03HD046599, P30HD003352)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- Alexander disease, astrocyte dysfunction, neurodegenerative diseases, astrocytes, neuroinflammation
- MeSH terms
- Animals, Astrocytes, Brain, Disease Models, Animal, Glial Fibrillary Acidic Protein, Humans, Models, Neurological, Neural Pathways, Age of Onset, Alexander Disease
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