Role of Pro-Inflammatory Cytokines Released from Microglia in Neurodegenerative Diseases
Open accessAbstract
Microglia are activated in response to a number of different pathological states within the CNS including injury, ischemia, and infection. Microglial activation results in their production of pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α. While release of these factors is typically intended to prevent further damage to CNS tissue, they may also be toxic to neurons and other glial cells. Mounting evidence indicates that chronic microglial activation may also contribute to the development and progression of neurodegenerative disorders. Unfortunately, determining the role of pro-inflammatory cytokines in these disorders has been complicated by their dual roles in neuroprotection and neurodegeneration. The purpose of this review is to summarize current understanding of the involvement of cytokines in neurodegenerative disorders and their potential signaling mechanisms in this context. Taken together, recent findings suggest that microglial activation and pro-inflammatory cytokines merit interest as targets in the treatment of neurodegenerative disorders.
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Microglial cells stimulate neuroinflammation by secreting TNF-α and IL-1β, as well as other interleukins.
“First, they stimulate neuroinflammation, secreting two main cytokines: tumor necrosis factor (TNF)-α and interleukin (IL)-1β, as well as other interleukins [75].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [75]
LPS induces production of TNF-α in the brain by microglial cells, which promotes BBB dysfunction and also causes neuronal cell death by phagocytosis.
“On the other hand, it has been shown that LPS induces the production of TNF-α in the brain by microglial cells, which promotes BBB dysfunction and also causes neuronal cell death by phagocytosis (Tanaka et al., 2006; Nishioku et al., 2010; Smith et al., 2012; Neniskyte et al., 2014).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Smith et al., 2012
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Retracted
- Authors
- Smith, J. A., Das, A., Ray, S. K., & Banik, N. L.
- Affiliations
- Medical University of South Carolina (US)
- University of South Carolina (US)
- Corresponding author
- Banik, Naren L.
- Venue
- Brain Research Bulletin
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 87
- Issue
- 1
- Pages
- 10-20
- ISSN
- 0361-9230 (ISSN-L)
- PMC
- PMC9827422
- OpenAlex
- W2054675033
- Cited by
- 1,165
- References
- 197
- Citations by year
- 2026: 117 · 2025: 143 · 2024: 107 · 2023: 91 · 2022: 90 · 2021: 85 · 2020: 77 · 2019: 61 · 2018: 72 · 2017: 51 · 2016: 66 · 2015: 59 · 2014: 59 · 2013: 60 · 2012: 26
- FWCI
- 4.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research Bulletin (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (NIH)
- National Institute of Neurological Disorders and Stroke (NINDS) (NS-31622, NS-38146, NS-41088)
- State of South Carolina Spinal Cord Injury Research Fund
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- microglial activation, inflammatory cytokines, neurodegenerative diseases, interleukin-1, interleukin-6, TNF-α, neuroinflammation, neuroprotection, neurodegeneration, cytokine signaling, therapeutic target
- MeSH terms
- Animals, Humans, Inflammation, Sympathetic Nervous System, Signal Transduction, Cytokines, Microglia, Neurodegenerative Diseases
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.
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