ArticleActa neuropathologica communications2018
Forced turnover of aged microglia induces an intermediate phenotype but does not rebalance CNS environmental cues driving priming to immune challenge.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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.
The trial behind it
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Who cites it
84 citing papers in PubMed, 144 citations in OpenAlex.
- Engineering mRNA-LNP Medicines for the Ageing Brain: Opportunities and Challenges for Neurodegenerative Diseases.Exploration (Beijing, China) · 2026Review
- The role of supraoptic hypothalamic arginine vasopressin neurons in aging-associated water balance and thermoregulatory deficits in male mice.Nature communications · 2026Article
- Aging effects on emotionality, cognition and brain mononuclear cells in Sprague-Dawley rats of both sexes.npj aging · 2026Article
- A Novel Central-Peripheral Interface: The Auditory Nerve Glial Transition Zone Exhibits Enhanced Age-Related Immune and Glial Cell Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Dysfunction of lipid metabolism and lysosomal capacity: at the core of microglial aging?Frontiers in aging neuroscience · 2026Review
- The auditory nerve glial transition zone is a focal site of age-related immune-myelin interactions.Frontiers in immunology · 2026Article
- Reprogramming microglia in sepsis-associated encephalopathy: from pathological dysfunction to therapeutic restoration.Frontiers in immunology · 2026Review
- Influenza A infection accelerates disease-associated microglia formation during physiological aging.bioRxiv : the preprint server for biology · 2025Article
- Inflammation associated microglial expansion disrupts hippocampal glial network communication, driving postoperative neurocognitive impairment.Journal of neuroinflammation · 2025Article
- Microglial Replacement Reverses Age-Associated Epigenetic Modifications Despite Accelerating Epigenetic Age.Aging and disease · 2025Article
- SkeletAge: Transcriptomics-based Aging Clock Identifies 26 New Targets in Skeletal Muscle Aging.bioRxiv : the preprint server for biology · 2025Article
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Human longevity and Alzheimer's disease variants act via microglia and oligodendrocyte gene networks.Brain : a journal of neurology · 2025Article
- Diffuse Traumatic Brain Injury Induced Stimulator of Interferons (STING) Signaling in Microglia Drives Cortical Neuroinflammation, Neuronal Dysfunction, and Impaired Cognition.Research square · 2025Article
- Proliferating Microglia Exhibit Unique Transcriptional and Functional Alterations in Alzheimer's Disease.ASN neuro · 2025Article
- Long-term reprogramming of primed microglia after moderate inhibition of CSF1R signaling.Glia · 2025Article
- Partial microglial depletion and repopulation exert subtle but differential effects on amyloid pathology at different disease stages.Scientific reports · 2024Article
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Novel microglial transcriptional signatures promote social and cognitive deficits following repeated social defeat.Communications biology · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Microglia are the resident innate immune cells of the central nervous system. Limited turnover throughout the lifespan leaves microglia susceptible to age-associated dysfunction. Indeed, we and others have reported microglia develop a pro-inflammatory or "primed" profile with age, characterized by increased expression of inflammatory mediators (e.g., MHC-II, CD68, IL-1β). Moreover, immune challenge with lipopolysaccharide (LPS) causes an exaggerated and prolonged neuroinflammatory response mediated by primed microglia in the aged brain. Recent studies show colony-stimulating factor 1 receptor (CSF1R) antagonism results in rapid depletion of microglia without significant complications. Therefore, we hypothesized that CSF1R antagonist-mediated depletion of microglia in the aged brain would result in repopulation with new and unprimed microglia. Here we provide novel evidence that microglia in the brain of adult (6-8 weeks old) and aged (16-18 months old) BALB/c mice were depleted following 3-week oral PLX5622 administration. When CSF1R antagonism was stopped, microglia repopulated equally in the adult and aged brain. Microglial depletion and repopulation reversed age-associated increases in microglial CD68
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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.