ArticleCommunications biology2024
Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Current Advances in the Physiological Roles of the Thioredoxin-Like Family of Selenoproteins.Biological trace element research · 2026Review
- Proteomic signatures of protected APOE ε4 carriers reveal causal pathways associated with delayed Alzheimer's disease onset.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Proteomic Signatures of ProtectedmedRxiv : the preprint server for health sciences · 2026Article
- Shared Risk Genes and Casual Relationships across Sex Hormone Related Traits and Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2026Article
- Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026Review
- Spatial Changes in Hippocampal Transcriptomic Profiles Following Limbic Non-convulsive Status Epilepticus: Insights into Long-Term Inflammation and Cognitive Deficits.Molecular neurobiology · 2026Article
- Neuroprotective effect of selenium in rats subjected to chronic intermittent cold and immobilization stress: The role of phosphorylated tau.Iranian journal of basic medical sciences · 2026Article
- Tau-Targeted Therapeutic Strategies: Mechanistic Targets, Clinical Pipelines, and Analysis of Failures.Cells · 2025Review
- Translational selenium nanomedicine synergizes with nab-paclitaxel to enhance antitumor effects in esophageal squamous cell cancer via selenoprotein N-mediated ER stress.Journal of nanobiotechnology · 2025Article
- Selenium and Selenoproteins: Mechanisms, Health Functions, and Emerging Applications.Molecules (Basel, Switzerland) · 2025Review
- The ubiquitin-proteasome system in Alzheimer's disease: mechanism of action and current status of treatment.Frontiers in aging neuroscience · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Lower selenium levels are observed in Alzheimer's disease (AD) brains, while supplementation shows multiple benefits. Selenoprotein W (SELENOW) is sensitive to selenium changes and binds to tau, reducing tau accumulation. However, whether restoration of SELENOW has any protective effect in AD models and its underlying mechanism remain unknown. Here, we confirm the association between SELENOW downregulation and tau pathology, revealing SELENOW's role in promoting tau degradation through the ubiquitin‒proteasome system. SELENOW competes with Hsp70 to interact with tau, promoting its ubiquitination and inhibiting tau acetylation at K281. SELENOW deficiency leads to synaptic defects, tau dysregulation and impaired long-term potentiation, resulting in memory deficits in mice. Conversely, SELENOW overexpression in the triple transgenic AD mice ameliorates memory impairment and tau-related pathologies, featuring decreased 4-repeat tau isoform, phosphorylation at Ser396 and Ser404, neurofibrillary tangles and neuroinflammation. Thus, SELENOW contributes to the regulation of tau homeostasis and synaptic maintenance, implicating its potential role in AD.
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