Cited by 1,287Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsTryptophan and brain disorders

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The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases

MCGEER, P, MCGEER, E·1995·Brain Research Reviews

DOI 10.1016/0165-0173(95)00011-9

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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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“LGI3 protein expression in astrocyte cultures (Fig. 4), clearly supporting our initial findings that LGI3 expression was induced by Aβ (Fig. 1). Many studies have shown that astrocytes are affected by soluble neuronal factors and several inflammationassociated cytokines (Eddleston and Mucke, 1993 ;M arket al., 1995; M…”
Background
Polymorphisms of the Macrophage Inhibitory Factor and C-Reactive Protein Genes in Subjects with Alzheimer’s Dementia
Flex, A., Pola, R., Serricchio, M., Gaetani, E., Proia, A. S., Giorgio, A. D., Papaleo, P., Bernabei, R., & Pola, P. (2004) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000080026 · Cited by 15
Modulation of the Production of Reactive Oxygen Species by Pre-Activated Neutrophils by Aminoadamantane Derivatives
Albrecht-Goepfert, E., Schempp, H., & Elstner, E. F. (1998) · Biochemical Pharmacology · doi:10.1016/s0006-2952(98)00024-0 · Cited by 15
The TGF‐β1/Upstream Stimulatory Factor‐Regulated PAI‐1 Gene:Potential Involvement and a Therapeutic Target in Alzheimer′sDisease
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“PAI-1 immunoreactivity in the central nervous system of AD patients was associated with senile plaques and ghost tangle structures [13] consistent with the earlier colocalization of PA and PAI-1 in plaque structures [14] which are sites of sustained inflammation [15].”
Background
Nonviral DNA Vaccination Augments Microglial Phagocytosis of β-Amyloid Deposits as a Major Clearance Pathway in an Alzheimer Disease Mouse Model
Okura, Y., Kohyama, K., Park, I.-K., & Matsumoto, Y. (2008) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31818b48db · Cited by 15
“Previously, microglia were thought to be harmful and toxic to neurons in the AD brain because there were sustained inflammatory responses, including complement activation (27).”
Background
Different Glial Reactions to Hippocampal Stab Wounds in Young Adult and Aged Rats
Zhu, W., Umegaki, H., Shinkai, T., Kurotani, S., Suzuki, Y., Endo, H., & Iguchi, A. (2003) · The Journals of Gerontology Series A · doi:10.1093/gerona/58.2.b117 · Cited by 15
“It has been well documented that activated microglia and astrocytes are involved in cytotoxic and inflammatory processes in neurodegenerative diseases as well as during the aging process (1,4,5,11).”
Background
Targeting APP metabolism for the treatment of Alzheimer's disease
Sambamurti, K., Hardy, J., Refolo, L. M., & Lahiri, D. K. (2002) · Drug Development Research · doi:10.1002/ddr.10077 · Cited by 14
Paeoniflorin ameliorates Aβ-stimulated neuroinflammation via regulation of NF-κB signaling pathway and Aβ degradation in C6 glial cells
Cho, E. J., Kim, H. Y., & Lee, A. Y. (2020) · Nutrition Research and Practice · doi:10.4162/nrp.2020.14.6.593 · Cited by 14
“Aβ-mediated neuroinflammation is an important mechanism that contributes to AD progression [20].”
Background
Naproxen as a potential candidate for promoting rivastigmine anti-Alzheimer activity against aluminum chloride-prompted Alzheimer's-like disease in rats; neurogenesis and apoptosis modulation as a possible underlying mechanism
Abdel‐Aal, R. A., Hussein, O. A., Elsaady, R. G., & Abdelzaher, L. A. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.174695 · Cited by 17
Disrupted Ultradian Activity Rhythms and Differential Expression of Several Clock Genes in Interleukin-6-Deficient Mice
Monje, F. J., Cicvaric, A., Aguilar, J. P. A., Elbau, I., Horváth, O., Diao, W., Glat, M., & Pollak, D. D. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00099 · Cited by 14
Protective Effect of Human-Neural-Crest-Derived Nasal Turbinate Stem Cells against Amyloid-β Neurotoxicity through Inhibition of Osteopontin in a Human Cerebral Organoid Model of Alzheimer’s Disease
Lim, J. Y., Lee, J. E., Park, S. A., Park, S., Yon, J.-M., Park, J.-A., Jeun, S., Kim, S. J., Lee, H. J., Kim, S. W., et al. (2022) · Cells · doi:10.3390/cells11061029 · Cited by 15
Advanced Contrast Agents for Multimodal Biomedical Imaging Based on Nanotechnology
Calle, D., Ballesteros, P., & Cerdán, S. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-7531-0_26 · Cited by 15
Non-steroidal anti-inflammatory agents, tolmetin and sulindac attenuate quinolinic acid (QA)-induced oxidative stress in primary hippocampal neurons and reduce QA-induced spatial reference memory deficits in male Wistar rats
Dairam, A., Müller, A. C., & Daya, S. (2007) · Life Sciences · doi:10.1016/j.lfs.2007.01.006 · Cited by 14
New Triterpenoids from the Tubers ofCorydalis ternata:Structural Elucidation and Bioactivity Evaluation
Kim, K., Lee, I., Choi, S., Lee, J. H., Moon, E., Kim, S. Y., & Lee, K. R. (2011) · Planta Medica · doi:10.1055/s-0030-1270781 · Cited by 14
Microglia: Roles of Microglia in Chronic Neurodegenerative Diseases
Wood, P. L. (2003) · Humana Press eBooks · doi:10.1385/1-59259-297-x:003 · Cited by 14
Can We Teach Old Dogs New Tricks? Neuroprotective Cell Therapy in Alzheimer's and Parkinson's Disease
Kazmerova, Z., Žilka, N., Cente, M., Neradil, P., Žilková, M., & Novák, M. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130572 · Cited by 14
“AD therapeutic approaches are predominantly focused on the elimination of the main pathological hallmarks: extracellular amyloid plaque and intracellular neurofibrillary tangle formation, synaptic and neuronal loss, and occurrence of strong neuroinflammation [89–96].”
Background
Access of HTB, main metabolite of triflusal, to cerebrospinal fluid in healthy volunteers
Valle, M., Barbanoj, M. J., DONNER, A., Izquierdo, I., Herranz, U., Klein, N., Eichler, H., Müller, M., & Brunner, M. (2005) · European Journal of Clinical Pharmacology · doi:10.1007/s00228-004-0887-0 · Cited by 14
“Furthermore, an increase in the levels of inflammationassociated proteins and in markers of oxidative stress, together with the activation of the complement system, indicate a state of chronic inflammation in the brain of patients with AD [1, 2].”
Background
Neuronal c-Abl activation leads to induction of cell cycle and interferon signaling pathways
Schlatterer, S. D., Suh, H.-S., Conejero‐Goldberg, C., Chen, S., Acker, C. M., Lee, S. C., & Davies, P. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-208 · Cited by 15
“Chronic neuroinflammation and upregulation of a multitude of cytokines has been shown to occur in AD [16-26].”
Background
Roles of CNS Macrophages in Neurodegeneration
Wood, P. L. (1998) · Humana Press eBooks · doi:10.1007/978-1-59259-473-3_1 · Cited by 14
Potential biomarkers for dementia in Trinidad and Tobago
Davis, G. K., Baboolal, N. S., Seales, D., Ramchandani, J., McKell, S., & McRae‐Degueurce, A. (2007) · Neuroscience Letters · doi:10.1016/j.neulet.2007.07.011 · Cited by 14
Effect of transforming growth factor-β1 on microglial MHC-class II expression
Pázmány, T., Kosa, J. P., Tomasi, T. B., Mechtler, L. L., Turoczı, A., & Lehotzky, A. (2000) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(99)00169-1 · Cited by 14
Biological Markers for Alzheimer's Disease
Tapiola, T. (2001) · Cited by 14
The Role of Chemokines in the Pathogenesis of Multiple Sclerosis
Woodroofe, M. N., Cross, A. K., Harkness, K. A., & Simpson, J. E. (1999) · Advances in experimental medicine and biology · doi:10.1007/978-1-4615-4685-6_11 · Cited by 14
The therapeutic potential and efficiency of Intracerebroventricular transplantation and intravenous injection of Mesenchymal stem cells in relieving Aß hallmarks and improving cognitive dysfunction in AD induced model
Anwar, M. M., Ali, O. S. M., Rashed, L. A., Badawi, A. M., & Eltablawy, N. A. (2021) · Gene Reports · doi:10.1016/j.genrep.2021.101323 · Cited by 13
Design and Synthesis of 6‐O‐Phosphorylated Heparan Sulfate Oligosaccharides to Inhibit Amyloid β Aggregation
Uchimura, K., Nishitsuji, K., Chiu, L., Ohgita, T., Saito, H., Allain, F., Gannedi, V., Wong, C., & Hung, S. (2022) · ChemBioChem · doi:10.1002/cbic.202200191 · Cited by 13
Osteoarthritis, osteoarthritis treatment and risk of incident dementia: a prospective cohort study based on UK Biobank
Guo, R., Ou, Y., Ma, L., Tang, L., Yang, L., Feng, J., Cheng, W., Tan, L., & Yu, J. (2024) · Age and Ageing · doi:10.1093/ageing/afae167 · Cited by 13
A dibenzoylmethane derivative protects against hydrogen peroxide-induced cell death and inhibits lipopolysaccharide-induced nitric oxide production in cultured rat astrocytes
Takano, K., Sugita, K., Moriyama, M., Hashida, K., Hibino, S., Choshi, T., Murakami, R., Yamada, M., Suzuki, H., Hori, O., et al. (2011) · Journal of Neuroscience Research · doi:10.1002/jnr.22617 · Cited by 13
The three sisters of fate: Genetics, pathophysiology and outcomes of animal models of neurodegenerative diseases
Klonarakis, M., Vos, M. D., Woo, E. K., Ralph, L. T., Thacker, J. S., & Gil‐Mohapel, J. (2022) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104541 · Cited by 14
EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer’s Disease
Khavinson, V. K., Linkova, N. S., Kozhevnikova, E. O., & Trofimova, S. (2020) · Molecules · doi:10.3390/molecules26010159 · Cited by 13
“Microglia or monocytes interaction with β-amyloid fibrils in AD activates a signaling cascade involving tyrosine kinase, which leads to the stimulation of gene expression of pro-inflammatory cytokines [81].”
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Effects of the Combined Treatment of Naloxone and Indomethacin on Catecholamines and Behavior After Intranigral Lipopolysaccharide Injection
Wang, V., Chia, L., Ni, D.-R., Cheng, L., Ho, Y.-P., Cheng, F., & Hong, J. (2004) · Neurochemical Research · doi:10.1023/b:nere.0000013736.80749.4b · Cited by 13
Nitric oxide inhibits the proliferation of murine microglial MG5 cells by a mechanism involving p21 but independent of p53 and cyclic guanosine monophosphate
Kawahara, K., Gotoh, T., Oyadomari, S., Kuniyasu, A., Kohsaka, S., Mori, M., & Nakayama, H. (2001) · Neuroscience Letters · doi:10.1016/s0304-3940(01)02079-1 · Cited by 13
Engagement of the Scavenger Receptor Is Not Responsible for β-Amyloid Stimulation of Monocytes to a Neurocytopathic State
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Blood levels of cytokines highlight the role of inflammation in Alzheimer's disease
Campanelli, L., Galeano, P., Prestia, F. A., Cuesta, C., Dalmasso, M. C., Flores-López, M., Gona, C., Irureta, N., Kairiyama, C., Lisso, J., et al. (2025) · Heliyon · doi:10.1016/j.heliyon.2025.e41725 · Cited by 16
Alzheimer’s: A Progressive Brain Disease: Causes, Symptoms, and Prevention
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Prognostic Value of Gut Microbiome for Conversion from Mild Cognitive Impairment to Alzheimer’s Disease Dementia within 4 Years: Results from the AlzBiom Study
Laske, C., Müller, S., Munk, M. H. J., Honold, I., Willmann, M., Peter, S., & Schoppmeier, U. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25031906 · Cited by 13
Untitled work
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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)
DOI: 10.1016/0165-0173(95)00011-9
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases

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