Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
Open accessAbstract
Neuroinflammation is associated with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Microglia and astrocytes are key regulators of inflammatory responses in the central nervous system. The activation of microglia and astrocytes is heterogeneous and traditionally categorized as neurotoxic (M1-phenotype microglia and A1-phenotype astrocytes) or neuroprotective (M2-phenotype microglia and A2-phenotype astrocytes). However, this dichotomized classification may not reflect the various phenotypes of microglia and astrocytes. The relationship between these activated glial cells is also very complicated, and the phenotypic distribution can change, based on the progression of neurodegenerative diseases. A better understanding of the roles of microglia and astrocytes in neurodegenerative diseases is essential for developing effective therapies. In this review, we discuss the roles of inflammatory response in neurodegenerative diseases, focusing on the contributions of microglia and astrocytes and their relationship. In addition, we discuss biomarkers to measure neuroinflammation and studies on therapeutic drugs that can modulate neuroinflammation.
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Recent scientific approaches, such as single-cell RNA sequencing, have revealed that glial cells have multiple reactive phenotypes related to their regional location and the type and stage of neurodegenerative diseases.
“However, the recent scientific approaches, such as single-cell RNA sequencing, have revealed that these glial cells have multiple reactive phenotypes related to their regional location and the type and stage of neurodegenerative diseases they are in ref. 275”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [275]
The Background states that microglia and astrocytes have multiple reactive phenotypes associated with disease type, stage, and regional location. Our copy does not say that single-cell RNA sequencing revealed these phenotypes, so the claim's attribution of that finding to the method is unsupported. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn AD, chronic release of DAMPs, mitochondrial DAMPs, and pro-inflammatory molecules contributes to onset and progression of neurodegeneration.
“in AD, the chronic release of DAMPs, mitochondrial-released DAMPs and pro-inflammatory molecules contributes to the onset and progression of neurodegeneration [57, 76, 97, 149, 194, 270, 304, 333, 345]”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [194]
The Background > AD section says neuroinflammation contributes to AD pathogenesis and that Aβ activates glial cells to release mediators that promote neurodegeneration. The Background section also says sustained inflammatory responses can lead to neurodegenerative diseases. Our copy does not identify chronic release of DAMPs or mitochondrial DAMPs as the mechanism in AD, so those specific parts of the claim are unsupported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredGlial cells are the primary cells involved in neuroinflammation and neurodegeneration.
“As we have discussed above, glial cells are the primary cells involved in neuroinflammation and neurodegeneration. Their crucial function in the development and progression of neurodegenerative diseases has also been elaborated in many reviews in the past year.275,468,469”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [275]
Chronic neuroinflammation mediated by disease-associated activation of microglia and astrocytes is a common pathological hallmark of neurodegeneration.
“Another common pathological hallmark of neurodegeneration appears to be chronic neuroinflammation, mediated by disease-associated activation of microglia and astrocytes [1].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [1]
Early neuroinflammation is protective as it promotes tissue repair, cellular debris clearance, and pathogen removal.
“Early neuroinflammation is protective as it promotes tissue repair, cellular debris clearance, and pathogen removal.117”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [117]
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- Authors
- Kwon, H. S., & Koh, S.-H.
- Affiliations
- Hanyang University (KR)
- Corresponding author
- Koh, Seong-Ho
- Venue
- Translational Neurodegeneration
- Published
- 2020-11-26
- Volume
- 9
- Issue
- 1
- Pages
- 42-42
- ISSN
- 2047-9158 (ISSN-L)
- PMC
- PMC7689983
- OpenAlex
- W3107395714
- Cited by
- 2,595
- References
- 125
- Citations by year
- 2026: 411 · 2025: 643 · 2024: 669 · 2023: 457 · 2022: 297 · 2021: 114
- FWCI
- 21.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Ministry of Science, ICT and Future Planning (2018R1A2A2A15023219)
- Ministry of Health and Welfare (grant number: HI20C0253)
- Medical Research Centre (2017R1A5A2015395)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- neuroinflammation, neurodegenerative diseases, microglia, astrocytes, glial activation, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, neuroinflammation biomarkers
- MeSH terms
- Animals, Astrocytes, Humans, Inflammation, Microglia, Inflammation Mediators, Neurodegenerative Diseases
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