Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis
Open accessAbstract
Dominant mutations in superoxide dismutase cause amyotrophic lateral sclerosis (ALS), an adult-onset neurodegenerative disease that is characterized by the loss of motor neurons. Using mice carrying a deletable mutant gene, diminished mutant expression in astrocytes did not affect onset, but delayed microglial activation and sharply slowed later disease progression. These findings demonstrate that mutant astrocytes are viable targets for therapies for slowing the progression of non-cell autonomous killing of motor neurons in ALS.
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Selectively deleting mutant SOD1 transgene expression in astrocytes sharply slows disease progression in the SOD1 mouse model of ALS.
“Selectively deleting mutant SOD1 transgene expression in astrocytes, sharply slows the disease progression in the SOD1 mouse model of ALS [22].”
From Distinct repertoires of microRNAs present in mouse astrocytes compared to astrocyte-secreted exosomes (2017) · cites this paper as [22]
In pre-symptomatic mutant SOD1 transgenic mice, activated microglia initially display neuroprotective properties that slow disease progression.
“In pre-symptomatic mutant SOD1 transgenic mice, activated microglia initially display neuroprotective properties that slow disease progression;”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [436]
In mutant SOD1 transgenic mice, continued unabridged neuroinflammation enhances neurodegeneration and accelerates disease progression.
“however, with time the continued and unabridged neuroinflammation only enhances neurodegeneration and accelerates disease progression [434–436].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [436]
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- Authors
- Yamanaka, K., Chun, S. J., Boillee, S., Fujimori-Tonou, N., Yamashita, H., Gutmann, D. H., Takahashi, R., Misawa, H., & Cleveland, D. W.
- Affiliations
- University of California San Diego (US)
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Yamanaka, Koji
- Cleveland, Don W
- Venue
- Nature Neuroscience
- Published
- 2008-02-03
- Volume
- 11
- Issue
- 3
- Pages
- 251-253
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3137510
- OpenAlex
- W2068147651
- Cited by
- 1,140
- References
- 15
- Citations by year
- 2026: 29 · 2025: 30 · 2024: 40 · 2023: 68 · 2022: 50 · 2021: 46 · 2020: 60 · 2019: 63 · 2018: 66 · 2017: 71 · 2016: 64 · 2015: 77 · 2014: 86 · 2013: 72 · 2012: 77
- FWCI
- 51.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS 27036, R37NS027036, R01NS027036)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- astrocytes, amyotrophic lateral sclerosis, superoxide dismutase 1, SOD1 mutations, non-cell autonomous neurodegeneration, motor neuron degeneration, microglial activation, disease progression, astrocyte-targeted therapy, mouse model
- MeSH terms
- Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Disease Models, Animal, Genes, Dominant, Glial Fibrillary Acidic Protein, Gliosis, Humans, Mice, Transgenic, Mutation, Nerve Degeneration, Nitric Oxide, Spinal Cord, Superoxide Dismutase, Genetic Therapy, Survival Rate, Cell Death, Microglia, Oxidative Stress, Disease Progression, Integrases, Mice, Nitric Oxide Synthase Type II
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