Evidence map›Paper›PMID 28226226›Full record

ReviewAnnual review of immunology2017

Microglia Function in the Central Nervous System During Health and Neurodegeneration.

Marco Colonna, Oleg Butovsky

Registry-linked trialAbstract readReview
In one paragraph

Review in Annual review of immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06489548 (Assessment of Foralumab Safety and Modulation of Microglial Activation Evaluated by PET Imaging in Patients With Early Symptomatic Alzheimer's Disease), which is not on this map. Cited by 1,688 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,688citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

NCT06489548 phase2recruitingnot on this mapstarted 2025, after this paper: background citation

Assessment of Foralumab Safety and Modulation of Microglial Activation Evaluated by PET Imaging in Patients With Early Symptomatic Alzheimer's Disease

TypeinterventionalSponsorBrigham and Women's HospitalRan2025 to 2026Enrolled16ConditionsDementia, Alzheimers Disease, Mild Cognitive Impairment Due to Alzheimer's DiseaseArmsForalumab TZLS-401 50 µg, Foralumab TZLS-401 100 µg
3 · Its place in the literature

Who cites it

1,688 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Oxytocin as regulator of stress and inflammation in aging.Neuroscience and biobehavioral reviews · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. IL-17D reprograms CD93Cellular & molecular immunology · 2026
    Article
  18. Article
  19. Review
  20. Article

1,628 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110; email: mcolonna@pathology.wustl.edu.
Oleg ButovskyAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; email: obutovsky@rics.bwh.harvard.edu.

Funding

Targeting TGFb/IFNy-IRF8 Signaling to Modulate Monocytes and their Crosstalk with Microglia and Astrocytes to Treat Multiple SclerosisR01NS088137 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Oleg Butovsky · 2014 to 2026
$4.9M
TREM2 IN MICROGLIA BIOLOGY AND ALZHEIMER'S DISEASERF1AG051485 · NIA · WASHINGTON UNIVERSITY · PI COLONNA, MARCO · 2015 to 2021
$3.5M
Microglial mechanisms of postoperative CNS inflammation and cognitive declineR01AG051812 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI BUTOVSKY, OLEG, CROSBY, GREGORY · 2016 to 2020
$2.7M
NIA NIH HHS R01 AG051812NIA NIH HHS RF1 AG051485NINDS NIH HHS R01 NS088137
6 · The paper itself

Abstract

Microglia are resident cells of the brain that regulate brain development, maintenance of neuronal networks, and injury repair. Microglia serve as brain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phenotype and tight regulation by the central nervous system (CNS) microenvironment. They are responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and other particulate and soluble antigens that may endanger the CNS. Furthermore, as the primary source of proinflammatory cytokines, microglia are pivotal mediators of neuroinflammation and can induce or modulate a broad spectrum of cellular responses. Alterations in microglia functionality are implicated in brain development and aging, as well as in neurodegeneration. Recent observations about microglia ontogeny combined with extensive gene expression profiling and novel tools to study microglia biology have allowed us to characterize the spectrum of microglial phenotypes during development, homeostasis, and disease. In this article, we review recent advances in our understanding of the biology of microglia, their contribution to homeostasis, and their involvement in neurodegeneration. Moreover, we highlight the complexity of targeting microglia for therapeutic intervention in neurodegenerative diseases.

Indexed as

Central Nervous SystemNeurogenic InflammationAnimalsBiological TherapyBrainCytokinesHomeostasisHumansMicrogliaNeurodegenerative DiseasesCytokineshomeostasismicroglianeurodegenerationphenotypesreceptorsregulation

Identifiers

PMID28226226
PMCPMC8167938

What OpenQuestion holds

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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.