Cited by 207Neuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular DisturbancesNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index.

Macrophages and Microglia in Central Nervous System Injury: Are They Helpful or Harmful?

Schwartz, Michal·2003·Journal of Cerebral Blood Flow & Metabolism

Abstract

Inflammation has been widely perceived as participating in the etiology of acute and chronic neurodegenerative conditions. Accordingly, in the context of traumatic injuries or chronic neurodegenerative diseases in the central nervous system (CNS), activated microglia have been viewed as detrimental and attempts have been made to treat both conditions by antiinflammatory therapy. Recent studies have suggested that microglia act as stand- by cells in the service of both the immune and the nervous systems. In the healthy CNS these cells are quiescent, but in the event of injury to axons or cell bodies they exercise their neural function by buffering harmful self-compounds and clearing debris from the damaged site, and their immune function by providing immune-related requirements for recovery. Proper regulation of the inflammatory (autoimmune) response to injury will arrest degeneration and promote regrowth, whereas inappropriate regulation will lead to ongoing degeneration. Regulation is achieved by the operation of a T cell-mediated response directed to abundant self-antigens residing in the damaged site. Since this immune-dependent mechanism was found to protect against glutamate toxicity (a major factor in neurodegenerative disorders), boosting of this response might constitute the basis for development of a therapeutic vaccination against neurodegenerative diseases, all of which exhibit similar pathways and patterns of progression.

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Crossref · 10.1097/00004647-200304000-00001

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Research works printed but not linked: 4

  1. Bracken, 1991, J Neurotrauma, 8, S47
  2. Faden, 1993, Crit Rev Neurobiol, 7, 175
  3. Medawar, 1948, Br J Exp Pathol, 29, 58
  4. Srebro, 2001, Folia Med Cracov, 42, 113

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Metadata

Authors
Schwartz, M.
Affiliations
Weizmann Institute of Science (IL)
Corresponding author
Schwartz, Michal
Venue
Journal of Cerebral Blood Flow & Metabolism
Published
2003-04
Volume
23
Issue
4
Pages
385-394
ISSN
0271-678X (ISSN-L)
OpenAlex
W1990064978
Cited by
207
References
103
Citations by year
2026: 3 · 2024: 6 · 2023: 6 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 5 · 2017: 6 · 2016: 9 · 2015: 8 · 2014: 4 · 2013: 11 · 2012: 13
FWCI
8.57
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, macrophages, central nervous system injury, neuroinflammation, neurodegenerative diseases, traumatic brain injury, T cell immunity, autoantigens, glutamate excitotoxicity, therapeutic vaccination, neuroprotection, axonal injury
MeSH terms
Animals, Central Nervous System Diseases, Humans, Macrophages, Microglia

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