ArticleFrontiers in cellular neuroscience2014
Microglia change from a reactive to an age-like phenotype with the time in culture.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis 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
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.
- Palmitoylethanolamide: A Nutritional Approach to Keep Neuroinflammation within Physiological Boundaries-A Systematic Review.International journal of molecular sciences · 2020Pooled it
- RAS modulation prevents progressive cognitive impairment after experimental stroke: a randomized, blinded preclinical trial.Journal of neuroinflammation · 2018Trial
- P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics.Brain : a journal of neurology · 2026Article
- Metabolic reprogramming is critical to microglial activation in Huntington's disease.JCI insight · 2026Article
- Live cell imaging of exogenous α-synuclein fibrils in primary microglia and neuron co-cultures.Biochemistry and biophysics reports · 2026Article
- Article
- Human amyotrophic lateral sclerosis/motor neuron disease: The disease-associated microglial pathway is upregulated while APOE genotype governs risk and survival.Brain pathology (Zurich, Switzerland) · 2025Article
- Loss of MFE-2 impairs microglial lipid homeostasis and drives neuroinflammation in Alzheimer's pathogenesis.Nature aging · 2025Article
- The Anti-Inflammatory Actions of Soluble Klotho in Brain Aging and Its Main Associated Diseases.International journal of molecular sciences · 2025Review
- Cpeb1 remodels cell type-specific translational program to promote fear extinction.Science advances · 2025Article
- Exosomes enriched with miR-124-3p show therapeutic potential in a new microfluidic triculture model that recapitulates neuron-glia crosstalk in Alzheimer's disease.Frontiers in pharmacology · 2025Article
- Aging of neural stem cells and vascular dysfunction: mechanisms, interconnection, and therapeutic perspectives.Cerebral circulation - cognition and behavior · 2025Review
- Up-regulated succinylation modifications induce a senescence phenotype in microglia by altering mitochondrial energy metabolism.Journal of neuroinflammation · 2024Article
- The Hidden Dangers of Sedentary Living: Insights into Molecular, Cellular, and Systemic Mechanisms.International journal of molecular sciences · 2024Review
- Current methods for the microglia isolation: Overview and comparative analysis of approaches.Cell and tissue research · 2024Review
- HIV-1 mRNA knockdown with CRISPR/CAS9 enhances neurocognitive function.Journal of neurovirology · 2024Article
- HIV-1 mRNA Knockdown with CRISPR/Cas9 Enhances Neurocognitive Function.Research square · 2023Article
- Microglial Metabolic Reprogramming: Emerging Insights and Therapeutic Strategies in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2023Review
- Microglia isolation from aging mice for cell culture: A beginner's guide.Frontiers in cellular neuroscience · 2023Article
- Senescence: A DNA damage response and its role in aging and Neurodegenerative Diseases.Frontiers in aging · 2023Review
40 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related neurodegenerative diseases have been associated with chronic neuroinflammation and microglia activation. However, cumulative evidence supports that inflammation only occurs at an early stage once microglia change the endogenous characteristics with aging and switch to irresponsive/senescent and dystrophic phenotypes with disease progression. Thus, it will be important to have the means to assess the role of reactive and aged microglia when studying advanced brain neurodegeneration processes and age-associated related disorders. Yet, most studies are done with microglia from neonates since there are no adequate means to isolate degenerating microglia for experimentation. Indeed, only a few studies report microglia isolation from aged animals, using either short-term cultures or high concentrations of mitogens in the medium, which trigger microglia reactivity. The purpose of this study was to develop an experimental process to naturally age microglia after isolation from neonatal mice and to characterize the cultured cells at 2 days in vitro (DIV), 10 DIV, and 16 DIV. We found that 2 DIV (young) microglia had predominant amoeboid morphology and markers of stressed/reactive phenotype. In contrast, 16 DIV (aged) microglia evidenced ramified morphology and increased matrix metalloproteinase (MMP)-2 activation, as well as reduced MMP-9, glutamate release and nuclear factor kappa-B activation, in parallel with decreased expression of Toll-like receptor (TLR)-2 and TLR-4, capacity to migrate and phagocytose. These findings together with the reduced expression of microRNA (miR)-124, and miR-155, decreased autophagy, enhanced senescence associated beta-galactosidase activity and elevated miR-146a expression, are suggestive that 16 DIV cells mainly correspond to irresponsive/senescent microglia. Data indicate that the model represent an opportunity to understand and control microglial aging, as well as to explore strategies to recover microglia surveillance function.
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.