ReviewInflammopharmacology2020
Microglial polarization: novel therapeutic mechanism against Alzheimer's disease.
Review in Inflammopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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.
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Who cites it
91 citing papers in PubMed, 148 citations in OpenAlex.
- Effect of MALT1 inhibition by MI‑2 on the microglial phenotype switch, inflammatory cytokine secretion, neuronal loss and oxidative stress in Alzheimer's disease.International journal of molecular medicine · 2026Article
- Cell-based immunotherapy for neurodegenerative disease: A promising avenue.Neural regeneration research · 2026Article
- Microglia-targetedMaterials today. Bio · 2026Article
- Oxyberberine-nanoparticle attenuates the cognitive deficits in a transgenic mouse model of Alzheimer's disease via modulating gut microbiota through suppressing CXCL10/CXCR3 pathway.Acta pharmacologica Sinica · 2026Article
- Nanomedicine targeting neuroinflammatory pathways in Alzheimer's disease: a new frontier in inflammopharmacology.Inflammopharmacology · 2026Review
- An engineered ROS-responsive cascade nanoplatform delays Alzheimer's disease progression via Nrf2/GPX4-mediated microglial functional reprogramming.Materials today. Bio · 2026Article
- Integrated Transcriptomic and Spatial Analyses Associate M2-like Myeloid Signatures with Neuroimmune Remodeling in Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Acupuncture as a modulator of microglial polarization and pyroptosis in depression: evidence from a chronic unpredictable mild stress rat model.Metabolic brain disease · 2026Article
- Interleukin-6, CD8Frontiers in aging neuroscience · 2026Review
- Targeting Adipocyte Enhancer-Binding Protein 1 to Induce Microglial Phenotype Shift for Immunotherapy in Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Targeting Multilayered Metabolic Networks in Brain Diseases: Emerging Perspectives on Nanodelivery Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Probenecid relieves LPS-induced neuroinflammation by modulating the NLRP1 inflammasome pathway in BV2 cells.Scientific reports · 2025Article
- Overexpression of TGFBR3 Aggravates Cognitive Impairment and Neuroinflammation by Promoting Microglia M1 Polarization in the APP/PS1 Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Inhibitory Potential of the Drimane Sesquiterpenoids Isotadeonal and Polygodial in the NF-kB Pathway.Molecules (Basel, Switzerland) · 2025Article
- Review
- From Genetics to Neuroinflammation: The Impact of ApoE4 on Microglial Function in Alzheimer's Disease.Cells · 2025Review
- 18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile.Cellular and molecular life sciences : CMLS · 2025Article
- Anesthesia-induced developmental neurotoxicity in the setting of systemic inflammation: the role of microglia.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- A specific and adaptable approach to track CD206Theranostics · 2025Article
- Glycolytic reprogramming during microglial polarization in neurological diseases.Frontiers in immunology · 2025Review
31 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most prevalent neurodegenerative disease that results in progressive dementia, and exhibits high disability and fatality rates. Recent evidence has demonstrated that neuroinflammation is critical in the pathophysiological processes of AD, which is characterized by the activation of microglia and astrocytes. Under different stimuli, microglia are usually activated into two polarized states, termed the classical 'M1' phenotype and the alternative 'M2' phenotype. M1 microglia are considered to promote inflammatory injury in AD; in contrast, M2 microglia exert neuroprotective effects. Imbalanced microglial polarization, in the form of excessive activation of M1 microglia and dysfunction of M2 microglia, markedly promotes the development of AD. Furthermore, an increasing number of studies have shown that the transition of microglia from the M1 to M2 phenotype could potently alleviate pathological damage in AD. Hence, this article reviews the current knowledge regarding the role of microglial M1/M2 polarization in the pathophysiology of AD. In addition, we summarize several approaches that protect against AD by altering the polarization states of microglia. This review aims to contribute to a better understanding of the pathogenesis of AD and, moreover, to explore the potential of novel drugs for the treatment of AD in the future.
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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.