Abstract
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. (Figure presented.) 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.
Original language | English |
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Pages (from-to) | 653-693 |
Number of pages | 41 |
Journal | Journal of Neurochemistry |
DOIs | |
State | Published - Sep 1 2016 |
Bibliographical note
Funding Information:Donovan Low, Kazuyuki Takata and Florent Ginhoux thank Dr Lucy Robison for editing the manuscript. Terrence Town acknowledges support from NIH R01 NS076794, an Alzheimer's Association Zenith Fellows Award (ZEN-10-174633), an American Federation of Aging Research/Ellison Medical Foundation Julie Martin Mid-Career Award in Aging Research (M11472), and a Cure Alzheimer's Fund Award, as well as startup funds from the Zilkha Neurogenetic Institute, which helped to make this work possible. M. Kerry O'Banion acknowledges support from NIH R21 NS048522, NIH R01 AG30149, and awards from the Killian J. and Caroline F. Schmitt Foundation Program on Integrative Brain Research. Bruce Lamb acknowledges support from NIH R01AG023012, NIH R01NS074804, Alzheimer's Association and BrightFocus Foundation. Marco Colonna is supported by Cure Alzheimer's Fund (CAF) and NIH RF1 AG051485 01. Gary Landreth acknowledges support trom the Alzheimer's Association, and NIH R01AG043522. Clive Holmes received funding from Pfizer pharmaceuticals for some of the clinical trial work. Katrin I. Andreasson acknowledges support from NIH R01AG030209, NIH R21AG033914, NIH P50 AG047366, Alzheimer's Association, American Federation for Aging Research, Bright Focus. Clive Holmes and Jessica Teeling acknowledge funding from the Wellcome Trust and the Alzheimer's Society UK. Marina Lynch acknowledges support from Science Foundation Ireland (11/PI/2014) and the Higher Education Authority, Ireland. Linda J. Van Eldik and Adam D. Bachstetter acknowledge support from NIH R01 NS093920, U01 AG050636, P30 AG028383, K99 AG044445, and grants from the Alzheimer's Association, Alzheimer's Drug Discovery Foundation, Kentucky Spinal Cord & Head Injury Research Trust (KSCHIRT), and Thome Memorial Foundation. Milos Pekny acknowledges support from the Swedish Medical Research Council (project 11548), AFA Research Foundation, ALF Göteborg (project 11392), Sten A. Olsson Foundation for Research and Culture, Hjärnfonden, Hagströmer's Foundation Millennium, the Swedish Stroke Foundation, Amlöv's Foundation, NanoNet COST Action (BM1002), the EU FP 7 Program EduGlia (237956), and the EU FP 7 Program TargetBraIn (279017). All experiments were conducted with the ARRIVE guidelines.
Publisher Copyright:
© 2016 International Society for Neurochemistry
Keywords
- Alzheimer disease
- Venusberg Neuroinflammation Meeting Bonn 2015
- blood–brain barrier
- innate immunity
- macrophage
- non-steroidal anti-inflammatory drugs (NSAIDs)
ASJC Scopus subject areas
- Biochemistry
- Cellular and Molecular Neuroscience