ArticleProceedings of the National Academy of Sciences of the United States of America2019
Amyloid-beta impairs TOM1-mediated IL-1R1 signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- TOM1 family proteins: from cargo sorting to immune dysregulation and cancer.Cell communication and signaling : CCS · 2026Review
- Microglial Deletion of Hrh4 Alleviates Alzheimer's Disease Pathologies by Enhancing Microglial Phagocytosis of Amyloid-β and Tau.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Network-level organization of systemic inflammation reflects early Alzheimer's-like behavioral changes.Scientific reports · 2025Article
- A TOM1 variant impairs interaction with TOLLIP, autophagosome-lysosome fusion and regulation of innate immunity.Disease models & mechanisms · 2025Article
- SENP1: A perspective from immune cells to disease (Review).Oncology reports · 2025Review
- The manipulator behind "Scissors": γ -secretase and its modulators in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Article
- The Therapeutic Prospects of Targeting IL-1R1 for the Modulation of Neuroinflammation in Central Nervous System Disorders.International journal of molecular sciences · 2022Review
- Interleukin-1β mediates alterations in mitochondrial fusion/fission proteins and memory impairment induced by amyloid-β oligomers.Journal of neuroinflammation · 2021Article
- Inflammatory Cytokine IL-1β Downregulates Endothelial LRP1 via MicroRNA-mediated Gene Silencing.Neuroscience · 2021Article
- Development of Tinnitus and Hyperacusis in a Mouse Model of Tobramycin Cochleotoxicity.Frontiers in molecular neuroscience · 2021Article
- Protein Trafficking or Cell Signaling: A Dilemma for the Adaptor Protein TOM1.Frontiers in cell and developmental biology · 2021Review
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Reply to Peng and Zhao: Loss of endocytic protein TOM1 in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Reduction in TOM1 expression exacerbates Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Human-Induced Neurons from Presenilin 1 Mutant Patients Model Aspects of Alzheimer's Disease Pathology.International journal of molecular sciences · 2020Article
- Review
- A Novel Mouse Model of Aminoglycoside-Induced Hyperacusis and Tinnitus.Frontiers in neuroscience · 2020Article
Corrections and comments
- Commented on by
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- Erratum issued
Authors and funding
20 authors.
Funding
Abstract
Defects in interleukin-1β (IL-1β)-mediated cellular responses contribute to Alzheimer's disease (AD). To decipher the mechanism associated with its pathogenesis, we investigated the molecular events associated with the termination of IL-1β inflammatory responses by focusing on the role played by the target of Myb1 (TOM1), a negative regulator of the interleukin-1β receptor-1 (IL-1R1). We first show that TOM1 steady-state levels are reduced in human AD hippocampi and in the brain of an AD mouse model versus respective controls. Experimentally reducing TOM1 affected microglia activity, substantially increased amyloid-beta levels, and impaired cognition, whereas enhancing its levels was therapeutic. These data show that reparation of the TOM1-signaling pathway represents a therapeutic target for brain inflammatory disorders such as AD. A better understanding of the age-related changes in the immune system will allow us to craft therapies to limit detrimental aspects of inflammation, with the broader purpose of sharply reducing the number of people afflicted by AD.
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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.