ArticleCNS neuroscience & therapeutics2024
Conditional knockout of AIM2 in microglia ameliorates synaptic plasticity and spatial memory deficits in a mouse model of Alzheimer's disease.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 17 citations in OpenAlex.
- Comparative insights into the apoptosome, inflammasomes and PIDDosome.Nature reviews. Immunology · 2026Review
- DNA Sensing Pathways in Innate Immunity: Implications for Alzheimer's Disease Progression and Therapy.Molecular neurobiology · 2026Review
- Dysregulation of the Tau-Microtubule-End-Binding Protein Axis in Alzheimer's Disease and Related Tauopathies.International journal of molecular sciences · 2026Review
- Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model.The Journal of clinical investigation · 2026Article
- Tubuloside B Alleviates AβNeurotoxicity research · 2026Article
- Mitochondrial Dysfunction in the Inflammatory Process of Neurodegenerative Diseases.Biomedicines · 2026Review
- Monocolonization withMicrobiology spectrum · 2026Article
- Cyclooxygenase-1 deletion in 5 × FAD mice protects against microglia-induced neuroinflammation and mitigates cognitive impairment.Translational neurodegeneration · 2025Article
- MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Inflammasome-Mediated Neuroinflammation: A Key Driver in Alzheimer's Disease Pathogenesis.Biomolecules · 2025Review
- OPA1 Enhances Microglial Amyloid-β Clearance and Alleviates Cognitive Impairments in an Alzheimer's Disease Model.Aging and disease · 2025Article
- Mapping microglial mechanisms in Alzheimer's disease: a comprehensive analysis.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- AIM2-Driven Inflammation in Periodontitis: Mechanisms and Systemic Implications.Journal of inflammation research · 2025Article
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Conditional knockout of AIM2 in microglia ameliorates synaptic plasticity and spatial memory deficits in a mouse model of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- The roles of AIM2 in neurodegenerative diseases: insights and therapeutic implications.Frontiers in immunology · 2024Review
- Bibliometric analysis of pathological mechanisms in Alzheimer's disease: Applications based on mouse models.Journal of Alzheimer's disease reportsReview
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
aimsSynaptic dysfunction is a hallmark pathology of Alzheimer's disease (AD) and is strongly associated with cognitive impairment. Abnormal phagocytosis by the microglia is one of the main causes of synapse loss in AD. Previous studies have shown that the absence of melanoma 2 (AIM2) inflammasome activity is increased in the hippocampus of APP/PS1 mice, but the role of AIM2 in AD remains unclear.
methodsInjection of Aβ
resultsThe expression level of AIM2 was increased in AD mice, and overexpression of AIM2 induced synaptic and cognitive impairments in C57BL/6 mice, similar to AD mice. Elevated expression levels of AIM2 occurred in microglia in AD mice. Conditional knockout of microglial AIM2 rescued cognitive and synaptic dysfunction in AD mice. Excessive microglial phagocytosis activity of synapses was decreased after knockout of microglial AIM2, which was associated with inhibiting complement activation.
conclusionOur results demonstrated that microglial AIM2 plays a critical role in regulating synaptic plasticity and memory deficits associated with AD, providing a new direction for developing novel preventative and therapeutic interventions for this disease.
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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.