Microglia in Alzheimer's Disease: It's All About Context

Weitz, Tara M.; Town, Terrence

doi:10.1155/2012/314185

Cited by 95Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

Microglia in Alzheimer's Disease: It's All About Context

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Weitz, Tara M., Town, Terrence·2012·International Journal of Alzheimer's Disease

DOI 10.1155/2012/314185PMC PMC3388286

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Abstract

Neuroinflammation is now regarded as both an early event and prime mover in the pathobiology of Alzheimer disease (AD), a neurodegenerative disease that represents a growing public health threat. As the resident innate immune cells within the central nervous system, microglia are centrally positioned as key orchestrators of brain inflammation. It is now accepted that numerous forms of activated microglia exist. Furthermore, while some types of reactive microglia are detrimental, others can actually be beneficial. In the context of AD etiopathology, much debate surrounds whether these enigmatic cells play “good” or “bad” roles. In this article, we distill a complex clinical and experimental literature focused on the contribution of microglia to AD pathology and progression. A synthesis of the literature only seems possible when considering context– the conditions under which microglia encounter and mount immunological responses to AD pathology. In order to carry out these diverse contextual responses, a number of key receptors and signaling pathways are variously activated. It will be critically important for future studies to address molecular mediators that lead to beneficial microglial responses and therefore represent important therapeutic targets for AD.

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Microglia are brain-resident innate immune effector cells and are widely thought to be the key mediators of amyloid beta clearance.
“Microglia are brain-resident innate immune effector cells and are widely thought to be the key mediators of amyloid beta clearance [14–16].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [16]
The Introduction identifies microglia as brain-resident macrophages involved in innate immune responses. But section 4.1 says they are generally regarded as inefficient Aβ phagocytes, and section 6 reports evidence that brain-resident microglia may not significantly affect plaque clearance. The paper therefore does not support calling them the key mediators of Aβ clearance. (LLM, conf=0.88)
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[32]Qiao X Cummins DJ Paul SM Neuroinflammation-induced acceleration of amyloid deposition in the APPV717F transgenic mouse European Journal of Neuroscience 2001 14 3 474 482 11553297
[61]Town T Nikolic V Tan J The microglial “activation” continuum: from innate to adaptive responses Journal of Neuroinflammation 2005 2, article 24 PMC1298325 16259628
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Microglia convert aggregated amyloid-β into neurotoxic forms through the shedding of microvesicles
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Loading into Nanoparticles Improves Quercetin's Efficacy in Preventing Neuroinflammation Induced by Oxysterols
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Brain injury, neuroinflammation and Alzheimer's disease
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Innate Immunity Fights Alzheimer's Disease
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Sesquiterpene dimer (DSF-52) from Artemisia argyi inhibits microglia-mediated neuroinflammation via suppression of NF-κB, JNK/p38 MAPKs and Jak2/Stat3 signaling pathways
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Retinoids as potential targets for Alzheimer's disease
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Potential therapeutic roles of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease
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Targeting neuroinflammation in Alzheimer’s disease: evidence for NSAIDs and novel therapeutics
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Molecular Basis of Etiological Implications in Alzheimer’s Disease: Focus on Neuroinflammation
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Neuronal Pentraxin 2 predicts medial temporal atrophy and memory decline across the Alzheimer’s disease spectrum
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IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia
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“Because microglial activation by other inflammatory cytokines can lead to Aβ clearance in vivo [3, 16, 27], we hypothesized that IL-1β overexpression creates an environment in which the resident microglial population is sufficiently activated to become better phagocytes.”
Raised Serum Proinflammatory Cytokines in Alzheimer’s Disease with Depression
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Microglia Ontology and Signaling
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Role of P2X7 Receptor in an Animal Model of Mania Induced by D-Amphetamine
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GPR84 deficiency reduces microgliosis, but accelerates dendritic degeneration and cognitive decline in a mouse model of Alzheimer’s disease
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Loss of P2Y2 Nucleotide Receptors Enhances Early Pathology in the TgCRND8 Mouse Model of Alzheimer's Disease
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Molecular Signaling Mechanisms of Natural and Synthetic Retinoids for Inhibition of Pathogenesis in Alzheimer’s Disease
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Liver X receptors: Emerging therapeutic targets for Alzheimer's disease
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Cold-Inducible RNA-Binding Protein Is an Important Mediator of Alcohol-Induced Brain Inflammation
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Protective Role of Endogenous Ovarian Hormones Against Learning and Memory Impairments and Brain Tissues Oxidative Damage Induced by Lipopolysaccharide
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PET Imaging of Translocator Protein (18 kDa) in a Mouse Model of Alzheimer's Disease UsingN-(2,5-Dimethoxybenzyl)-2-18F-Fluoro-N-(2-Phenoxyphenyl)Acetamide
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The Effects of Age and Cx 3 cr1 Deficiency on Retinal Microglia in the Ins2 Akita Diabetic Mouse
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Periodontitis and alzheimer´s disease
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Xanthoceraside Inhibits Pro-inflammatory Cytokine Expression in Aβ25–35/IFN-γ–Stimulated Microglia Through the TLR2 Receptor, MyD88, Nuclear Factor-κB, and Mitogen-Activated Protein Kinase Signaling Pathways
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Centrally Delivered BACE1 Inhibitor Activates Microglia, and Reverses Amyloid Pathology and Cognitive Deficit in Aged Tg2576 Mice
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Decay in Retinoic Acid Signaling in Varied Models of Alzheimer’s Disease and In-Vitro Test of Novel Retinoic Acid Receptor Ligands (RAR-Ms) to Regulate Protective Genes
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Suppressive Effects of SuHeXiang Wan on Amyloid-β42-Induced Extracellular Signal-Regulated Kinase Hyperactivation and Glial Cell Proliferation in a Transgenic Drosophila Model of Alzheimer’s Disease
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The calcineurin inhibitor, Sarah/Nebula, exacerbates Aβ42 phenotypes in aDrosophilamodel of Alzheimer's disease
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A Global Immune Deficit in Alzheimer's Disease and Mild Cognitive Impairment Disclosed by a Novel Data Mining Process
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The Role of the Innate Immune System in Alzheimer’s Disease and Frontotemporal Lobar Degeneration: An Eye on Microglia
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Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer's Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion
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Mouse Hepatitis Virus Infection Upregulates Genes Involved in Innate Immune Responses
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Alternative Targets to Fight Alzheimer’s Disease: Focus on Astrocytes
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MyD88 Is Dispensable for Cerebral Amyloidosis and Neuroinflammation in APP/PS1 Transgenic Mice
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Towards early diagnosis of Alzheimer’s disease: advances in immune-related blood biomarkers and computational approaches
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Diphtheria toxoid nanoparticles improve learning and memory impairment in animal model of Alzheimer’s disease
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Depression, Diabetes and Dementia
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Protective Role of Endogenous Ovarian Hormones Against Learning and Memory Impairments and Brain Tissues Oxidative Damage Induced by
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PATHOGENIC ROLE OF MICROGLIA-DERIVED MICROVESICLES IN NEURODEGENERATION
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Die Rolle und Funktionsweise der Chemokinrezeptoren CXCR4 und CXCR7 in Mikroglia und Astrozyten
Lipfert, J. (2013) · Qucosa (Saxon State and University Library Dresden)
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doi:10.1155/2012/314185 Review Article Microglia in Alzheimer’s Disease: It’s All About Context
Weitz, T. M., & Town, T. (2012)
Self-citation
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Function of the microglia in neuroinflammation of Alzheimer's disease:a brief review
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Authors: Weitz, T. M., & Town, T.
Affiliations: Cedars-Sinai Medical Center (US)
Corresponding author: Town, Terrence
ORCID: Weitz, Tara M.
Venue: International Journal of Alzheimer's Disease
Publisher: Wiley
Published: 2012
Volume: 2012
Pages: 1-11
ISSN: 2090-0252 (ISSN-L)
2090-8024
DOI: 10.1155/2012/314185
PMC: PMC3388286
OpenAlex: W2114688326
Cited by: 95
References: 69
Citations by year: 2026: 2 · 2025: 4 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 5 · 2020: 2 · 2019: 8 · 2018: 4 · 2017: 5 · 2016: 8 · 2015: 15 · 2014: 16 · 2013: 19 · 2012: 3
FWCI: 8.54
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (unspecified)
Locations: International Journal of Alzheimer s Disease (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: National Institute on Aging (5R00AG029726-04, 1R01NS076794-01, ZEN-10-174633)
National Institute of Neurological Disorders and Stroke (5R00AG029726-04, 1R01NS076794-01, ZEN-10-174633)
Alzheimer’s Association (5R00AG029726-04, 1R01NS076794-01, ZEN-10-174633)
American Federation of Aging Research/Ellison Medical Foundation Julie Martin Mid-Career Award (5R00AG029726-04, 1R01NS076794-01, ZEN-10-174633)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: microglia, Alzheimer's disease, neuroinflammation, reactive microglia, microglial activation, innate immunity, microglial receptors, signaling pathways, neurodegeneration, therapeutic target

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