Targeting innate immunity for neurodegenerative disorders of the central nervous system
Open accessAbstract
Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. This mini review series originated from the 4th Venusberg Meeting on Neuroinflammation held in Bonn, Germany, 7-9th May 2015, presenting updates on innate immunity in acute brain injury and chronic neurodegenerative disorders, such as traumatic brain injury and Alzheimer disease, on the role of astrocytes and microglia, as well as technical developments that may help elucidate neuroinflammatory mechanisms and establish clinical relevance. In this meeting report, a brief overview of physiological and pathological microglia morphology is followed by a synopsis on PGE2 receptors, insights into the role of arginine metabolism and further relevant aspects of neuroinflammation in various clinical settings, and concluded by a presentation of technical challenges and solutions when working with microglia and astrocyte cultures. Microglial ontogeny and induced pluripotent stem cell-derived microglia, advances of TREM2 signaling, and the cytokine paradox in Alzheimer's disease are further contributions to this article. Neuroinflammation is critically involved in numerous neurodegenerative diseases, and key signaling steps of innate immune activation hence represent promising therapeutic targets. This mini review series originated from the 4th Venusberg Meeting on Neuroinflammation held in Bonn, Germany, 7-9th May 2015, presenting updates on innate immunity in acute brain injury and chronic neurodegenerative disorders, such as traumatic brain injury and Alzheimer's disease, on the role of astrocytes and microglia, as well as technical developments that may help elucidate neuroinflammatory mechanisms and establish clinical relevance. In this meeting report, a brief overview on physiological and pathological microglia morphology is followed by a synopsis on PGE2 receptors, insights into the role of arginine metabolism and further relevant aspects of neuroinflammation in various clinical settings, and concluded by a presentation of technical challenges and solutions when working with microglia cultures. Microglial ontogeny and induced pluripotent stem cell-derived microglia, advances of TREM2 signaling, and the cytokine paradox in Alzheimer's disease are further contributions to this article.
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Transplanted iMGLs closely resemble quiescent microglia.
“closely resembling quiescent microglia”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Andreasson et al., 2016
TREM2 is a critical regulator of microglia and macrophage phenotype and is involved in neurodegenerative diseases.
“This receptor is a critical regulator of microglia and macrophage phenotype and is involved in neurodegenerative diseases (Andreasson et al., 2016).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Andreasson et al., 2016
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Fluid-percussion model of mechanical brain injury in the cat
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Dementia Resulting From Traumatic Brain Injury: What Is the Pathology?
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Microglial Dynamics and Role in the Healthy and Diseased Brain: A Paradigm of Functional Plasticity
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Progress toward the clinical application of patient-specific pluripotent stem cells
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HLA-haplotype banking and iPS cells
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Nitration of Tyrosine 10 Critically Enhances Amyloid β Aggregation and Plaque Formation
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Microglia and Alzheimer's disease pathogenesis
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COX-2 Inhibitors and Cardiovascular Risk
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Extended results of the Alzheimer's disease anti‐inflammatory prevention trial
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“…insulin-like growth factor-1 and PPAR signaling; in this screen, expression of RXRc was enhanced with ablation of microglial EP2, and RXRc along with its binding partner PPARc reduce pro-inflammatory gene expression (Heneka et al. 2007) and enhance clearance of Ab peptides (Yamanaka et al. 2012).”
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Self-citation
Flagged first, then by citations
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iPSC-derived human microglia-like cells to study neurological diseases
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CD4 T Cells Induce A Subset of MHCII-Expressing Microglia that Attenuates Alzheimer Pathology
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Isolation and Phenotyping of Adult Mouse Microglial Cells
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Human iPSC Models in Drug Discovery: Opportunities and Challenges
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- Authors
- Andreasson, K. I., Bachstetter, A. D., Colonna, M., Ginhoux, F., Holmes, C., Lamb, B., Landreth, G., Lee, D. C., Low, D., Lynch, M. A., Monsonego, A., O'Banion, M. K., Pekny, M., Puschmann, T., Russek‐Blum, N., Sandusky, L. A., Selenica, M. B., Takata, K., Teeling, J., Town, T., & Van Eldik, L. J.
- Affiliations
- Stanford Medicine (US)
- University of Kentucky (US)
- Washington University in St. Louis (US)
- Agency for Science, Technology and Research (SG)
- University of Southampton (GB)
- Cleveland Clinic (US)
- Case Western Reserve University (US)
- University of South Florida (US)
- Trinity College Dublin (IE)
- Ben-Gurion University of the Negev (IL)
- Departments of Neuroscience and Neurology Del Monte Neuromedicine Institute University of Rochester School of Medicine & Dentistry Rochester NY USA
- Florey Institute of Neuroscience and Mental Health (AU)
- University of Gothenburg (SE)
- Dead Sea and Arava Science Center (IL)
- Southampton General Hospital (GB)
- University of Southern California (US)
- Sanders‐Brown Center on Aging Spinal Cord and Brain Injury Research Center, and Department of Anatomy and Neurobiology University of Kentucky Lexington KY USA
- ORCID
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2016-08-24
- Volume
- 138
- Issue
- 5
- Pages
- 653-693
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC5433264
- OpenAlex
- W2418940280
- Cited by
- 126
- References
- 403
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 11 · 2023: 6 · 2022: 8 · 2021: 12 · 2020: 17 · 2019: 17 · 2018: 15 · 2017: 27 · 2016: 7
- FWCI
- 1.93
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- NOVA (University of Newcastle Australia) (submittedVersion)
- Funders
- National Institutes of Health (R01 NS076794, R21 NS048522, R01 AG30149, R01AG023012, R01NS074804, RF1 AG051485 01, R01AG043522, R01AG030209, R21AG033914, P50 AG047366, R01 NS093920, U01 AG050636, P30 AG028383, K99 AG044445)
- American Federation for Aging Research (M11472)
- Cure Alzheimer's Fund
- Alzheimer's Association
- Pfizer
- Wellcome Trust
- Science Foundation Ireland (11/PI/2014)
- Higher Education Authority
- Alzheimer's Drug Discovery Foundation
- Edward N. and Della L. Thome Memorial Foundation
- Medicinska Forskningsrådet (11548)
- Seventh Framework Programme (237956, 279017)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- neuroinflammation, innate immunity, neurodegenerative diseases, microglia, astrocytes, traumatic brain injury, Alzheimer's disease, PGE2 receptors, arginine metabolism, induced pluripotent stem cell-derived microglia, TREM2 signaling, microglial morphology
- MeSH terms
- Animals, Astrocytes, Central Nervous System, Humans, Immunity, Innate, Inflammation, Microglia, Neurodegenerative Diseases
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.
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