ReviewActa neuropathologica2014
The role of microglia in human disease: therapeutic tool or target?
Review in Acta neuropathologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 146 citations in OpenAlex.
- Prenatal opioid exposure and maternal HCV infection impair microglia development and function: A patient-specific in vitro model.Brain, behavior, and immunity · 2025Article
- Intranasal Delivery of Lithium Salt Suppresses Inflammatory Pyroptosis in the Brain and Ameliorates Memory Loss and Depression-like Behavior in 5XFAD Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Development of a rabbit model for adrenoleukodystrophy: A pilot study on gene therapy using rAAV9.Molecular therapy. Nucleic acids · 2025Article
- Satellite microglia: marker of traumatic brain injury and regulator of neuronal excitability.Journal of neuroinflammation · 2025Article
- Microglial dynamics and emerging therapeutic strategies in CNS homeostasis and pathology.Frontiers in pharmacology · 2025Review
- Pathology and Treatments of Alzheimer's Disease Based on Considering Changes in Brain Energy Metabolism Due to Type 2 Diabetes.Molecules (Basel, Switzerland) · 2024Review
- Synergistic label-free fluorescence imaging and miRNA studies reveal dynamic human neuron-glial metabolic interactions following injury.Science advances · 2024Article
- Intranasal Delivery of Lithium Salt Suppresses Inflammatory Pyroptosis in the brain and Ameliorates Memory Loss and Depression-like Behavior in 5XFAD mice.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic efficacy of intracerebral hematopoietic stem cell gene therapy in an Alzheimer's disease mouse model.Nature communications · 2024Article
- Alpha-synuclein inclusion responsive microglia are resistant to CSF1R inhibition.Journal of neuroinflammation · 2024Article
- The pathology of X-linked adrenoleukodystrophy: tissue specific changes as a clue to pathophysiology.Orphanet journal of rare diseases · 2024Review
- Microglia in Central Control of Metabolism.Physiology (Bethesda, Md.) · 2024Review
- Tagged IDS causes efficient and engraftment-independent prevention of brain pathology during lentiviral gene therapy for Mucopolysaccharidosis type II.Molecular therapy. Methods & clinical development · 2023Article
- Neurodegeneration and inflammation crosstalk: Therapeutic targets and perspectives.IBRO neuroscience reports · 2023Article
- Effect of Hematopoietic Stem Cell Transplantation and Post-Transplantation Cyclophosphamide on the Microglia Phenotype in Rats with Experimental Allergic Encephalomyelitis.Archivum immunologiae et therapiae experimentalis · 2023Article
- Gap Junctions and Connexins in Microglia-Related Oxidative Stress and Neuroinflammation: Perspectives for Drug Discovery.Biomolecules · 2023Review
- Review
- Age-Associated Glia Remodeling and Mitochondrial Dysfunction in Neurodegeneration: Antioxidant Supplementation as a Possible Intervention.Nutrients · 2022Review
- Brain Metabolic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- What microglia depletion approaches tell us about the role of microglia on synaptic function and behavior.Frontiers in cellular neuroscience · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia have long been the focus of much attention due to their strong proliferative response (microgliosis) to essentially any kind of damage to the CNS. More recently, we reached the realization that these cells play specific roles in determining progression and outcomes of essentially all CNS disease. Thus, microglia has ceased to be viewed as an accessory to underlying pathologies and has now taken center stage as a therapeutic target. Here, we review how our understanding of microglia's involvement in promoting or limiting the pathogenesis of diseases such as amyotrophic lateral sclerosis, Alzheimer's disease, Huntington's disease, multiple sclerosis, X-linked adrenoleukodystrophy (X-ALD) and lysosomal storage diseases (LSD) has changed over time. While strategies to suppress the deleterious and promote the virtuous functions of microglia will undoubtedly be forthcoming, replacement of these cells has already proven its usefulness in a clinical setting. Over the past few years, we have reached the realization that microglia have a developmental origin that is distinct from that of bone marrow-derived myelomonocytic cells. Nevertheless, microglia can be replaced, in specific situations, by the progeny of hematopoietic stem cells (HSCs), pointing to a strategy to engineer the CNS environment through the transplantation of modified HSCs. Thus, microglia replacement has been successfully exploited to deliver therapeutics to the CNS in human diseases such as X-ALD and LSD. With this outlook in mind, we will discuss the evidence existing so far for microglial involvement in the pathogenesis and the therapy of specific CNS disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.