ReviewCells2019
Molecular Mechanisms of Microglial Motility: Changes in Ageing and Alzheimer's Disease.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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.
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
79 citing papers in PubMed, 141 citations in OpenAlex.
- Epigenetic aging in Alzheimer's disease: Relation to proteome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Review
- Review
- Live-Cell Imaging of Microglia in Organotypic Brain Slices Using Microcontact Printing.Biomolecules · 2026Article
- Vessel-associated microglia are differentially activated and distributed in relation to systemic infection and Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Microglial Adaptations to Chronic Nicotine in the Cerebellum: Proteomic Evidence for Neuroimmune Vulnerability.Journal of proteome research · 2026Article
- The Arp2/3 complex controls the development of homeostatic microglia.EMBO reports · 2026Article
- Entorhinal Cholecystokinin in Alzheimer's Disease: Its Earliest Vulnerability and Rescue Effects Across Different Disease Stages in a Mouse Model.Cellular and molecular neurobiology · 2026Article
- TRPV4 Deficiency Shifts Mitochondrial Dynamics Toward a Fragmented Morphology in Primary Microglia.Cells · 2026Article
- Article
- Disease-associated RNA and protein signatures in iPSC-derived microglia model of Alzheimer's disease.Frontiers in neuroscience · 2026Article
- Non-invasive bioelectrical therapy suppresses retinal neovascularization by modulating cellular metabolism and inflammation.Cell communication and signaling : CCS · 2025Article
- RNA-binding protein IMP1/ZBP1 directs local translation in microglial processes to regulate motility and phagocytosis during inflammation.PLoS biology · 2025Article
- The chloride intracellular channel 1 (CLIC1) is essential for microglial morphodynamics and neuroinflammation.Science advances · 2025Article
- Cell autonomous microglia defects in a stem cell model of frontotemporal dementia tau.Molecular psychiatry · 2025Article
- Making tracks: microglia and the extracellular matrix.Molecular neurodegeneration · 2025Review
- Article
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- Targeting phagocytosis for amyloid-β clearance: implications of morphology remodeling and microglia activation probed by bifunctional chimaeras.Nature communications · 2025Article
- Prefrontal cortical microglial transcriptome relates to mouse offspring executive function deficits after perinatal opioid exposure in a sex-dependent manner.Brain, behavior, and immunity · 2025Article
19 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 1 country.
Funding
Abstract
Microglia are the tissue-resident immune cells of the central nervous system, where they constitute the first line of defense against any pathogens or injury. Microglia are highly motile cells and in order to carry out their function, they constantly undergo changes in their morphology to adapt to their environment. The microglial motility and morphological versatility are the result of a complex molecular machinery, mainly composed of mechanisms of organization of the actin cytoskeleton, coupled with a "sensory" system of membrane receptors that allow the cells to perceive changes in their microenvironment and modulate their responses. Evidence points to microglia as accountable for some of the changes observed in the brain during ageing, and microglia have a role in the development of neurodegenerative diseases, such as Alzheimer's disease. The present review describes in detail the main mechanisms driving microglial motility in physiological conditions, namely, the cytoskeletal actin dynamics, with emphasis in proteins highly expressed in microglia, and the role of chemotactic membrane proteins, such as the fractalkine and purinergic receptors. The review further delves into the changes occurring to the involved proteins and pathways specifically during ageing and in Alzheimer's disease, analyzing how these changes might participate in the development of this disease.
Indexed as
Identifiers
What OpenQuestion holds
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.