ReviewNature reviews. Neurology2014
Microglial priming in neurodegenerative disease.
Review in Nature reviews. Neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 649 papers, 3 of them syntheses that pooled 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.
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
649 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Pooled it
- Bibliometric analysis of neuroinflammation and Alzheimer's disease.Frontiers in aging neuroscience · 2024Pooled it
- Pooled it
- Short-chain fatty acid-producing commensals: Key modulators of AD neuroinflammation via the microbiota-gut-brain axis.Current research in microbial sciences · 2026Review
- Failure of Neuroinflammatory Resolution in Brain Aging: Molecular Mechanisms and an Integrative Framework of Microglial Inflammometabolic Locking.Molecular neurobiology · 2026Review
- Translational modelling of human microglia from cultures to chimeras.Experimental & molecular medicine · 2026Review
- Hospital-treated infection associated with Alzheimer's disease pathology: underlying mechanisms.Molecular psychiatry · 2026Review
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Article
- The Oral-Brain Axis: A Unified Framework Linking Trigeminal Sensorimotor Dysfunction, Chronic Stress, Neuroinflammation, and Neurodegeneration.International journal of molecular sciences · 2026Review
- Microglia heterogeneity in vascular dementia pathology.iScience · 2026Review
- An ApoE-Associated Low-Inflammatory Microglial State Emerges After Inflammatory Challenge in Alzheimer's Disease Mice.Neuroscience bulletin · 2026Article
- Targeting Mitochondrial Dysfunction in Microglia: A New Frontier for Treating Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Prenatal cigarette exposure induces offspring hyperactivity and affective alterations via gut -brain axis metabolic dysregulation and region-specific neuronal hyperactivation.Brain, behavior, & immunity - health · 2026Article
- Therapeutic Effects of Spent Ground Coffee Oil on Nociception, Anxiety- and Depression-Like Behaviors, and Inflammatory Mechanisms in a CFA-Induced Intraplantar Inflammation Model in Mice.Molecular neurobiology · 2026Article
- From Perinatal Stress to Schizophrenia: The Emerging Role of Glial Pathology.Annals of neurosciences · 2026Review
- A Vortioxetine-Glycyrrhizic Acid Supramolecular Complex: Synthesis and Cellular Effects on Microglial and Blood Cells Under Inflammatory and Glucocorticoid Challenge.Biomedicines · 2026Article
- Energy Homeostasis Disruption in Neurological Disorders: Mitochondrial Dysfunction, High-Energy Phosphate Transfer, and Extracellular ATP-Dependent Purinergic Dysregulation.International journal of molecular sciences · 2026Review
- The lung-brain axis in neurodegeneration: inflammatory, immune, and vascular mechanisms with therapeutic implications.Inflammopharmacology · 2026Review
- Epigenetic mechanisms of inflammatory memory in the central nervous system.Nature immunology · 2026Review
589 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.
Funding
Abstract
Under physiological conditions, the number and function of microglia--the resident macrophages of the CNS--is tightly controlled by the local microenvironment. In response to neurodegeneration and the accumulation of abnormally folded proteins, however, microglia multiply and adopt an activated state--a process referred to as priming. Studies using preclinical animal models have shown that priming of microglia is driven by changes in their microenvironment and the release of molecules that drive their proliferation. Priming makes the microglia susceptible to a secondary inflammatory stimulus, which can then trigger an exaggerated inflammatory response. The secondary stimulus can arise within the CNS, but in elderly individuals, the secondary stimulus most commonly arises from a systemic disease with an inflammatory component. The concept of microglial priming, and the subsequent exaggerated response of these cells to secondary systemic inflammation, opens the way to treat neurodegenerative diseases by targeting systemic disease or interrupting the signalling pathways that mediate the CNS response to systemic inflammation. Both lifestyle changes and pharmacological therapies could, therefore, provide efficient means to slow down or halt neurodegeneration.
Indexed as
Identifiers
24638131What 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.