Cited by 126Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsNeuroscience and Neuropharmacology Research

The brain’s best friend: microglial neurotoxicity revisited

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Hellwig, Sabine, Heinrich, Annette, Biber, Knut·2013·Frontiers in Cellular Neuroscience

Abstract

One long standing aspect of microglia biology was never questioned; their involvement in brain disease. Based on morphological changes (retracted processes and amoeboid shape) that inevitably occur in these cells in case of damage in the central nervous system, microglia in the diseased brain were called "activated." Because "activated" microglia were always found in direct neighborhood to dead or dying neuron, and since it is known now for more than 20 years that cultured microglia release numerous factors that are able to kill neurons, microglia "activation" was often seen as a neurotoxic process. From an evolutionary point of view, however, it is difficult to understand why an important, mostly post-mitotic and highly vulnerable organ like the brain would host numerous potential killers. This review is aimed to critically reconsider the term microglia neurotoxicity and to discuss experimental problems around microglia biology, that often have led to the conclusion that microglia are neurotoxic cells.

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Crossref · 10.3389/fncel.2013.00071

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  • Activated microglia support neuronal survival by engulfing pathogens, debris, and neurotoxic entities and by synthesizing neurotrophic factors, but excessive or sustained microglial activation produces inflammatory collateral damage and may fuel further injury.

    “Activated microglia also support neuronal survival and function by engulfing pathogens, cellular debris, or other neurotoxic entities and can synthesize various neurotrophic factors to promote tissue maintenance and repair (63, 64). However, the excessive or sustained activation of microglial cells (such as in chronic neurodegenerative diseases) usually produces significant inflammatory collateral”

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Authors
Hellwig, S., Heinrich, A., & Biber, K.
Affiliations
  • University of Freiburg (DE)
  • University Medical Center Groningen (NL)
Corresponding author
Biber, Knut
Venue
Frontiers in Cellular Neuroscience
Published
2013
Volume
7
Pages
71-71
ISSN
1662-5102 (ISSN-L)
OpenAlex
W2030448361
Cited by
126
References
173
Citations by year
2026: 1 · 2025: 2 · 2024: 5 · 2023: 8 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 14 · 2018: 9 · 2017: 13 · 2016: 16 · 2015: 17 · 2014: 15 · 2013: 5
FWCI
9.92
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, cc-by)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
Funders
  • Deutsche Forschungsgemeinschaft (BI 668/2-2, BI 668/5-1, DFG BI 668/5-1)
  • Bundesministerium für Bildung und Forschung
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
microglia, microglial neurotoxicity, microglial activation, microglial morphology, amoeboid microglia, neuroinflammation, brain disorders

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