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Cited by 258Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersTraumatic Brain Injury and Neurovascular Disturbances

Neuroinflammation: An Integrating Overview of Reactive‐Neuroimmune Cell Interactions in Health and Disease

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Kölliker-Frers, Rodolfo, Udovin, Lucas, Otero-Losada, Matilde, Kobiec, Tamara, Herrera, María Inés, Palacios, Jorge, Razzitte, Gabriela, Capani, Francisco·2021·Mediators of Inflammation
DOI 10.1155/2021/9999146PMC PMC8187052
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Abstract

The concept of central nervous system (CNS) inflammation has evolved over the last decades. Neuroinflammation is the response of reactive CNS components to altered homeostasis, regardless of the cause to be endogenous or exogenous. Neurological diseases, whether traumatic, neoplastic, ischemic, metabolic, toxic, infectious, autoimmune, developmental, or degenerative, involve direct and indirect immune‐related neuroinflammation. Brain infiltrates of the innate and adaptive immune system cells appear in response to an infective or otherwise noxious agent and produce inflammatory mediators. Mediators of inflammation include local and recruited cells and signals. Processes derived from extrinsic and intrinsic CNS diseases also elicit the CNS inflammatory response. A deeper understanding of immune‐related inflammation in health and disease is necessary to find potential therapeutic targets for preventing or reducing CNS damage. This review is aimed at discussing the innate and adaptive immune system functions and their roles in regulating brain cell responses in disease and homeostasis maintenance.

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  • NLRP3 inflammasome is particularly implicated in AD, activated by Aβ oligomers, driving caspase-1-dependent maturation of IL-1β and IL-18, thereby exacerbating neuronal damage.

    “Among them, the NLRP3 inflammasome is particularly implicated in AD, activated by Aβ oligomers, which drives caspase-1–dependent maturation of IL-1β and IL-18, thereby exacerbating neuronal damage [90].”

    From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [90]

    Section 3.1 discusses IL-1β in CNS inflammation and mentions inflammatory processes in Alzheimer's disease, but it does not connect either to NLRP3. Searches of our copy for NLRP3, Aβ oligomers, caspase-1, IL-18, and inflammasome did not find the claimed activation pathway or its effect on neuronal damage. The retrieved passages have no page numbers. (LLM, conf=0.76)

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Sorted by citations

Authors
Kölliker-Frers, R., Udovin, L., Otero-Losada, M., Kobiec, T., Herrera, M. I., Palacios, J., Razzitte, G., & Capani, F.
Affiliations
  • Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
  • Hospital Ramos Mejía (AR)
ORCID
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2021-01
Volume
2021
Issue
1
Pages
9999146-9999146
ISSN
  • 0962-9351 (ISSN-L)
  • 1466-1861
DOI
10.1155/2021/9999146
PMC
PMC8187052
OpenAlex
W3166870166
Cited by
258
References
17
Citations by year
2026: 77 · 2025: 82 · 2024: 58 · 2023: 25 · 2022: 13 · 2021: 2
FWCI
2.92
Type
journal article
Language
en
Open access
Licence
Locations
  • Mediators of Inflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Conicet (submittedVersion, cc-by-nc-sa)
  • Greater South Information System
Funders
  • Agencia Nacional de Promoción Científica y Tecnológica (2085)
  • Consejo Nacional de Investigaciones Científicas y Técnicas
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
neuroinflammation, neuroimmune interactions, innate immune system, adaptive immunity, inflammatory mediators, neurological disorders, neurodegenerative diseases
MeSH terms
Neuroinflammatory Diseases, Animals, Hypoxia, Astrocytes, Autophagy, Brain, Central Nervous System, Central Nervous System Diseases, Fibrosis, Homeostasis, Humans, Immune System, Inflammation, Neuroimmunomodulation, Microglia, Oxidative Stress, Inflammation Mediators, Adaptive Immunity

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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