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Macrophages and Microglia in Central Nervous System Injury: Are They Helpful or Harmful?
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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“Reports have shown that exercise (cycling) can increase plasma levels of the anti-inflammatory cytokine IL-10 in individuals with PD along with improved motor performance.111, 112”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [111]
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Cardoso, A. L., Guedes, J. R., Pereira de Almeida, L., & Pedroso de Lima, M. C. (2012) · Immunology · doi:10.1111/j.1365-2567.2011.03514.x · Cited by 336
Metadata
- Authors
- Schwartz, M.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Schwartz, Michal
- ORCID
- Schwartz, Michal
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- 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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