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Cited by 573Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsNF-κB Signaling Pathways

Inflammatory Response in the CNS: Friend or Foe?

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Sochocka, Marta, Diniz, Breno Satler, Leszek, Jerzy·2017·Molecular Neurobiology
DOI 10.1007/s12035-016-0297-1PMC PMC5684251
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Abstract

Inflammatory reactions could be both beneficial and detrimental to the brain, depending on strengths of their activation in various stages of neurodegeneration. Mild activation of microglia and astrocytes usually reveals neuroprotective effects and ameliorates early symptoms of neurodegeneration; for instance, released cytokines help maintain synaptic plasticity and modulate neuronal excitability, and stimulated toll-like receptors (TLRs) promote neurogenesis and neurite outgrowth. However, strong activation of glial cells gives rise to cytokine overexpression/dysregulation, which accelerates neurodegeneration. Altered mutual regulation of p53 protein, a major tumor suppressor, and NF-κB, the major regulator of inflammation, seems to be crucial for the shift from beneficial to detrimental effects of neuroinflammatory reactions in neurodegeneration. Therapeutic intervention in the p53-NF-κB axis and modulation of TLR activity are future challenges to cope with neurodegeneration.

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  • In AD, brain microglial cells are activated in response to Aβ and other neuropathological changes and undergo complex neuroinflammation processes, playing either a protective or detrimental role.

    “In AD, brain microglial cells are activated in response to Aβ and other neuropathological changes and undergo complex neuroinflammation processes,54 playing either a protective or detrimental role in the disease.55, 56”

    From Acoustofluidic assembly of 3D neurospheroids to model Alzheimer's disease (2020) · cites this paper as [55]

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Authors
Sochocka, M., Diniz, B. S., & Leszek, J.
Affiliations
  • Ludwik Hirszfeld Institute of Immunology and Experimental Therapy (PL)
  • The University of Texas Health Science Center at Houston (US)
  • Wroclaw Medical University (PL)
Corresponding author
Leszek, Jerzy
ORCID
Venue
Molecular Neurobiology
Publisher
Springer Science and Business Media LLC
Published
2016-11-26
Volume
54
Issue
10
Pages
8071-8089
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
DOI
10.1007/s12035-016-0297-1
PMC
PMC5684251
OpenAlex
W2554390311
Cited by
573
References
39
Citations by year
2026: 35 · 2025: 64 · 2024: 64 · 2023: 50 · 2022: 71 · 2021: 111 · 2020: 73 · 2019: 56 · 2018: 31 · 2017: 17
FWCI
3.04
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Neurobiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
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 › Cancer Research › NF-κB Signaling Pathways
Keywords
neuroinflammation, neurodegeneration, microglia, astrocytes, cytokines, Toll-like receptors, p53, NF-κB, neuroprotection, neurogenesis, synaptic plasticity, glial activation
MeSH terms
Animals, Astrocytes, Humans, Inflammation, Neurons, NF-kappa B, Microglia, Toll-Like Receptors

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.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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