The DOI matches its Crossref record; 311 of the 319 references it cites were found in a registry or an index.
The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Abstract
Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. New agents directed against the inflammatory processes revealed in studies of Alzheimer disease lesions may have broad therapeutic applications.
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“Despite not being modeled in the pathway enrichment analysis and the lack of reported evidence of their possible relationship with AD, these genes encode key products having relevant functions within the immune system, which seems to influence several neurodegenerative and mental diseases.57, 58”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [57]
In the citing paper
“This activation and consequent neuroinflammation are substantially involved in the progression of neurodegenerative diseases (McGeer and McGeer, 1995)”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as McGeer and McGeer, 1995
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Cited by
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Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Inflammation and Alzheimer’s disease
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Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253
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Metadata
- Authors
- MCGEER, P., & MCGEER, E.
- Affiliations
- University of British Columbia (CA)
- Corresponding author
- MCGEER, P
- Venue
- Brain Research Reviews
- Publisher
- Elsevier BV
- Published
- 1995-09
- Volume
- 21
- Issue
- 2
- Pages
- 195-218
- ISSN
- 0165-0173 (ISSN-L)
- OpenAlex
- W2090930997
- Cited by
- 1,287
- References
- 319
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 17 · 2023: 14 · 2022: 24 · 2021: 19 · 2020: 16 · 2019: 18 · 2018: 27 · 2017: 29 · 2016: 19 · 2015: 29 · 2014: 46 · 2013: 42 · 2012: 36
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer Society of B.C.
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- neuroinflammation, Alzheimer's disease, neurodegenerative diseases, microglia, astrocytes, complement system, inflammatory cytokines, acute phase proteins, chronic inflammation, anti-inflammatory therapy, indomethacin, anti-inflammatory agents, neuroprotection
- MeSH terms
- Alzheimer Disease, Brain, Humans, Inflammation, Nerve Degeneration, Nervous System Diseases
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