The role of immune-mediated alterations and disorders in ALS disease
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that leads to neuronal death in the brain and spinal cord. Over the last decades, evidence has emerged regarding the functional diversity of astrocytes, microglia, and T cells in the central nervous system (CNS), and the role of neuroinflammation in ALS. In this review, we summarize current knowledge regarding neuroinflammation in ALS, both at the level of specific molecular pathways and potential cellular pathways as well as outline questions about the immune mechanisms involved in ALS pathogenesis.
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mSOD1 microglia may contribute to the progression of ALS, and SOD1G93A increases the expression of the pro-inflammatory pattern recognition receptor RAGE and releases HMGB1- and SOD1-rich exosomes that promote pro-inflammatory responses.
“Rodrigues et al. (90) found that mSOD1 microglia may contribute to the progression of ALS and that SOD1G93A increased the expression of the pro-inflammatory pattern recognition receptor RAGE, as well as releasing HMGB1- and SOD1-rich exosomes that promote pro-inflammatory responses.”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [90]
Alterations to the gut bacteria indirectly affect the ratio of macrophages to microglia.
“Alterations to the gut bacteria indirectly affect the ratio of macrophages to microglia”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [90]
M1 (pro-inflammatory) microglia produce ROS and pro-inflammatory cytokines such as NO, IL-1β, IL-6, TNF-α, and IFN-γ.
“with M1 (pro-inflammatory) microglia producing ROS and pro-inflammatory cytokines such as NO, IL-1β, IL-6, TNF-α, and IFN-γ”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [90]
M2 (anti-inflammatory)-like microglial cytoplasm is associated with production of anti-inflammatory cytokines such as IL-4, IL-10, and IL-13.
“and M2 (anti-inflammatory)-like microglial cytoplasm being associated with production of anti-inflammatory cytokines such as IL-4, IL-10, and IL-13 (28, 90).”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [90]
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Flagged first, then by citations
Research works printed but not linked: 1
- [1]Mehta P, Kaye W, Raymond J, Punjani R, Larson T, Cohen J. Prevalence of Amyotrophic Lateral Sclerosis. Morb Mortal Wkly Rep. 2018; 67(46): 1285– 9. PMC6289079 30462626
Cited by
Sorted by citations
Hong, D., Zhang, C., Wu, W., Lu, X., & Zhang, L. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1133546 · Cited by 38 · see citing works
- Authors
- Rodrigues Lima-Junior, J., Sulzer, D., Lindestam Arlehamn, C. S., & Sette, A.
- Affiliations
- New York State Psychiatric Institute (US)
- La Jolla Institute for Immunology (US)
- Corresponding author
- Sette, Alessandro
- Venue
- Human Immunology
- Publisher
- Elsevier BV
- Published
- 2021-03
- Volume
- 82
- Issue
- 3
- Pages
- 155-161
- ISSN
- 0198-8859 (ISSN-L)
- PMC
- PMC7942756
- OpenAlex
- W3129758780
- Cited by
- 33
- References
- 103
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 6 · 2021: 2
- FWCI
- 0.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Human Immunology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Michael J Fox Foundation for Parkinson's Research
- NINDS
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- amyotrophic lateral sclerosis, neuroinflammation, immune-mediated neurodegeneration, astrocytes, microglia, T cells, ALS pathogenesis, neurodegeneration
- MeSH terms
- Amyotrophic Lateral Sclerosis, Animals, Brain, Humans, Immunity, Cellular, Neuroglia, Neurons, Spinal Cord, T-Lymphocytes, Signal Transduction, Autoimmunity, Neurogenic Inflammation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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