ArticleeLife2016
Microglia contribute to circuit defects in Mecp2 null mice independent of microglia-specific loss of Mecp2 expression.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
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Who cites it
96 citing papers in PubMed, 146 citations in OpenAlex.
- Translational modelling of human microglia from cultures to chimeras.Experimental & molecular medicine · 2026Review
- Maternal Immune Activation Leads to Lasting Sex-Specific Changes in Behavior and Hippocampal Morphological and Molecular Features in 12-Month-Old Rat Offspring.International journal of molecular sciences · 2026Article
- Sexual dimorphism of autism-like phenotypes in microglial eIF4E overexpression mice.bioRxiv : the preprint server for biology · 2026Article
- Juvenile influenza can impair myelin development and adult behavior through chemokine signaling in mice.bioRxiv : the preprint server for biology · 2026Article
- Diverse excess GABA modes drive autism and epilepsy-autism comorbidity.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Flipping the Switch: MeCP2-Mediated Lactylation Rewires Microglial Metabolism and Inflammation via the HK2/mTOR Axis in Poststroke Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Toward an NGF-based therapy for Rett syndrome.Frontiers in neuroscience · 2026Review
- A vicious cycle of microglial dysfunction: bridging synaptic pruning and neuroinflammation across the neurodevelopmental continuum.Frontiers in immunology · 2026Review
- Microglia: Mediators of experience-driven corrective neuroplasticity.IBRO neuroscience reports · 2025Article
- Glia Preserve Their Own Functions While Compensating for Neighboring Glial Cell Dysfunction.Glia · 2025Article
- Zebrafish in neurodevelopmental disorders studies: Genetic models and pathological involvement of microglia.Developmental medicine and child neurology · 2025Review
- The Role of Prenatal Microglial Activation and Its Sex Differences in the Development of Neuropsychiatric Disorders and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- AI-enabled drug prediction and gene network analysis reveal therapeutic use of vorinostat for Rett Syndrome in preclinical models.Communications medicine · 2025Article
- Altered Microglial Plasticity in the Periaqueductal Grey of Pre-Symptomatic Mecp2-Heterozygous Mice Following Early-Life Stress.Neuromolecular medicine · 2025Article
- MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- Early-Life Mild Traumatic Brain Injury Alters Neurodevelopment and Behavior in Mice.Neurotrauma reports · 2025Article
- Review
- Human microglial cells as a therapeutic target in a neurodevelopmental disease model.Stem cell reports · 2024Article
- Microglial over-pruning of synapses during development in autism-associated SCN2A-deficient mice and human cerebral organoids.Molecular psychiatry · 2024Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Microglia, the resident CNS macrophages, have been implicated in the pathogenesis of Rett Syndrome (RTT), an X-linked neurodevelopmental disorder. However, the mechanism by which microglia contribute to the disorder is unclear and recent data suggest that microglia do not play a causative role. Here, we use the retinogeniculate system to determine if and how microglia contribute to pathogenesis in a RTT mouse model, the Mecp2 null mouse (Mecp2(tm1.1Bird/y)). We demonstrate that microglia contribute to pathogenesis by excessively engulfing, thereby eliminating, presynaptic inputs at end stages of disease (≥P56 Mecp2 null mice) concomitant with synapse loss. Furthermore, loss or gain of Mecp2 expression specifically in microglia (Cx3cr1(CreER);Mecp2(fl/y)or Cx3cr1(Cr)(eER); Mecp2(LSL/y)) had little effect on excessive engulfment, synapse loss, or phenotypic abnormalities. Taken together, our data suggest that microglia contribute to end stages of disease by dismantling neural circuits rendered vulnerable by loss of Mecp2 in other CNS cell types.
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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.