ArticleAging cell2015
Enhanced microglial pro-inflammatory response to lipopolysaccharide correlates with brain infiltration and blood-brain barrier dysregulation in a mouse model of telomere shortening.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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
39 citing papers in PubMed, 68 citations in OpenAlex.
- Chandipura virus encephalitis: an emerging pediatric neurotropic threat in india-virology, epidemiology, pathogenesis, and public health challenges.Journal of neurovirology · 2026Review
- Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.bioRxiv : the preprint server for biology · 2025Article
- Telomerase Depletion Accelerates Ageing of the Zebrafish Brain.Aging cell · 2025Article
- Prematurely Aged Human Microglia Exhibit Impaired Stress Response and Defective Nucleocytoplasmic Shuttling of ALS Associated FUS.Aging cell · 2025Article
- Telomere-driven senescence accelerates tau pathology, neuroinflammation and neurodegeneration in a tauopathy mouse model.Acta neuropathologica communications · 2025Article
- Immunosenescence and age-related immune cells: causes of age-related diseases.Archives of pharmacal research · 2025Review
- The Role of Glia Telomere Dysfunction in the Pathogenesis of Central Nervous System Diseases.Molecular neurobiology · 2024Review
- Gut Metabolites Acting on the Gut-Brain Axis: Regulating the Functional State of Microglia.Aging and disease · 2024Review
- Evaluation of the Impact ofMolecules (Basel, Switzerland) · 2024Article
- Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology.Acta neuropathologica communications · 2023Article
- Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer's models.Cell reports · 2022Article
- Extension of the Life Span by Acarbose: Is It Mediated by the Gut Microbiota?Aging and disease · 2022Article
- Microbiota-microglia connections in age-related cognition decline.Aging cell · 2022Review
- Long-term male-specific chronic pain via telomere- and p53‑mediated spinal cord cellular senescence.The Journal of clinical investigation · 2022Article
- Age-dependent effects of gut microbiota metabolites on brain resident macrophages.Frontiers in cellular neuroscience · 2022Review
- Melatonin Reduces Neuroinflammation and Improves Axonal Hypomyelination by Modulating M1/M2 Microglia Polarization via JAK2-STAT3-Telomerase Pathway in Postnatal Rats Exposed to Lipopolysaccharide.Molecular neurobiology · 2021Article
- Early-life stress does not alter spatial memory performance, hippocampal neurogenesis, neuroinflammation, or telomere length in 20-month-old male mice.Neurobiology of stress · 2021Article
- Article
- Dysregulated non-coding telomerase RNA component and associated exonuclease XRN1 in leucocytes from women developing preeclampsia-possible link to enhanced senescence.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are a proliferative population of resident brain macrophages that under physiological conditions self-renew independent of hematopoiesis. Microglia are innate immune cells actively surveying the brain and are the earliest responders to injury. During aging, microglia elicit an enhanced innate immune response also referred to as 'priming'. To date, it remains unknown whether telomere shortening affects the proliferative capacity and induces priming of microglia. We addressed this issue using early (first-generation G1 mTerc(-/-) )- and late-generation (third-generation G3 and G4 mTerc(-/-) ) telomerase-deficient mice, which carry a homozygous deletion for the telomerase RNA component gene (mTerc). Late-generation mTerc(-/-) microglia show telomere shortening and decreased proliferation efficiency. Under physiological conditions, gene expression and functionality of G3 mTerc(-/-) microglia are comparable with microglia derived from G1 mTerc(-/-) mice despite changes in morphology. However, after intraperitoneal injection of bacterial lipopolysaccharide (LPS), G3 mTerc(-/-) microglia mice show an enhanced pro-inflammatory response. Nevertheless, this enhanced inflammatory response was not accompanied by an increased expression of genes known to be associated with age-associated microglia priming. The increased inflammatory response in microglia correlates closely with increased peripheral inflammation, a loss of blood-brain barrier integrity, and infiltration of immune cells in the brain parenchyma in this mouse model of telomere shortening.
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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.