Microglia: a sensor for pathological events in the CNS
Abstract
The most characteristic feature of microglial cells is their rapid activation in response to even minor pathological changes in the CNS. Microglia activation is a key factor in the defence of the neural parenchyma against infectious diseases, inflammation, trauma, ischaemia, brain tumours and neurodegeneration. Microglia activation occurs as a graded response in vivo. The transformation of microglia into potentially cytotoxic cells is under strict control and occurs mainly in response to neuronal or terminal degeneration, or both. Activated microglia are mainly scavenger cells but also perform various other functions in tissue repair and neural regeneration. They form a network of immune alert resident macrophages with a capacity for immune surveillance and control. Activated microglia can destroy invading micro-organisms, remove potentially deleterious debris, promote tissue repair by secreting growth factors and thus facilitate the return to tissue homeostasis. An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
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Changes in microglial density, morphology, and transcriptional state have been observed in postmortem brain tissue of patients with neurological and psychiatric disorders.
“For decades, changes in microglial density, morphology, and transcriptional state have been observed in postmortem brain tissue of patients with neurological and psychiatric disorders17–21.”
From Genetic analysis of the human microglial transcriptome across brain regions, aging and disease pathologies (2022) · cites this paper as [18]
Microglia become activated under brain injury and immunological stimuli and undergo alterations from a resting state to an active state.
“Microglia become activated under brain injury and immunological stimuli (Kreutzberg, 1996) and undergo several alterations from a “resting state” to an active state (Hanisch and Kettenmann, 2007; Kettenmann et al., 2011).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Kreutzberg, 1996
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- Authors
- Kreutzberg, G. W.
- Affiliations
- Max Planck Institute of Psychiatry (DE)
- Corresponding author
- Kreutzberg, Georg W
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 1996-08
- Volume
- 19
- Issue
- 8
- Pages
- 312-318
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W2109759840
- Cited by
- 4,396
- References
- 67
- Citations by year
- 2026: 37 · 2025: 63 · 2024: 71 · 2023: 82 · 2022: 104 · 2021: 144 · 2020: 159 · 2019: 126 · 2018: 158 · 2017: 167 · 2016: 161 · 2015: 169 · 2014: 217 · 2013: 216 · 2012: 227
- FWCI
- 11.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, microglial activation, CNS pathology, neuroinflammation, neurodegeneration, brain injury, immune surveillance, tissue repair, nerve regeneration, intercellular communication, glial reaction, neuroprotection
- MeSH terms
- Animals, Central Nervous System, Central Nervous System Diseases, Humans, Microglia
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