ArticleNeural regeneration research2023
TMEM16F may be a new therapeutic target for Alzheimer's disease.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Effect of MALT1 inhibition by MI‑2 on the microglial phenotype switch, inflammatory cytokine secretion, neuronal loss and oxidative stress in Alzheimer's disease.International journal of molecular medicine · 2026Article
- TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2026Review
- Microglia and neuroinflammation: An in-depth analysis from functional diversity to disease mechanisms.Clinical and translational medicine · 2026Review
- Niflumic acid suppresses NLRP3 inflammasome activation by limiting chloride efflux and mitochondrial ROS production.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A Humanized Knock-in Mouse Model of the PSEN1 V97L Mutation from a Major Chinese Alzheimer's Disease Pedigree Reveals Early Neuroinflammation.Neuroscience bulletin · 2026Article
- Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.Cell communication and signaling : CCS · 2026Review
- RRBP1 Inhibition Reduces Microglial M1 Polarization and Inflammation-Mediated Neuronal Loss and Oxidative Stress by Regulating ERK Pathway in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Article
- NLRP3 Inflammasome Triggers Inflammation of Obstructive Sleep Apnea.Current molecular medicine · 2025Review
- TMEM16F scramblase regulates angiogenesis via endothelial intracellular signaling.Journal of cell science · 2024Article
- TMEM16F exacerbates tau pathology and mediates phosphatidylserine exposure in phospho-tau-burdened neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Artemisinin reduces PTSD-like symptoms, improves synaptic plasticity, and inhibits apoptosis in rats subjected to single prolonged stress.Frontiers in pharmacology · 2024Article
- Mesenchymal and Neural Stem Cell-Derived Exosomes in Treating Alzheimer's Disease.Bioengineering (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TMEM16F is involved in many physiological processes such as blood coagulation, cell membrane fusion and bone mineralization. Activation of TMEM16F has been studied in various central nervous system diseases. High TMEM16F level has been also found to participate in microglial phagocytosis and transformation. Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer's disease. However, few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer's disease. In this study, we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD. We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome. Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice. After TMEM16F knockdown in mice, spatial memory ability was improved, microglia polarization to the M2 phenotype was promoted, NLRP3 inflammasome activation was inhibited, cell apoptosis and Aβ plaque deposition in brain tissue were reduced, and brain injury was alleviated. We used amyloid-beta (Aβ
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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 Socratic graph.