ArticleFrontiers in molecular neuroscience2020
Chronic Sodium Selenate Treatment Restores Deficits in Cognition and Synaptic Plasticity in a Murine Model of Tauopathy.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Fish consumption and cognitive function in aging: a systematic review of observational studies.GeroScience · 2026Pooled it
- Metabolic and redox modulation by 2-deoxy-D-glucose and sodium selenite protects against pentylenetetrazole-kindled seizures, neuroinflammation and cognitive dysfunction.Metabolic brain disease · 2026Article
- Hexaraphane as a potential therapeutic strategy for tauopathies.Redox biology · 2026Article
- Unveiling the Role of Selenium in Child Development: Impacts on Growth, Neurodevelopment and Immunity.Journal of clinical medicine · 2025Review
- The Role of Gut Microbiota in the Neuroprotective Effects of Selenium in Alzheimer's Disease.Molecular neurobiology · 2025Review
- New horizons for the role of selenium on cognitive function: advances and challenges.Metabolic brain disease · 2024Review
- Does modulation of tau hyperphosphorylation represent a reasonable therapeutic strategy for Alzheimer's disease? From preclinical studies to the clinical trials.Molecular psychiatry · 2023Review
- Revisiting the Role of Vitamins and Minerals in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Article
- Tauopathies: new perspectives and challenges.Molecular neurodegeneration · 2022Review
- "Don't Phos Over Tau": recent developments in clinical biomarkers and therapies targeting tau phosphorylation in Alzheimer's disease and other tauopathies.Molecular neurodegeneration · 2021Review
- Sodium selenate as a disease-modifying treatment for mild-moderate Alzheimer's disease: an open-label extension study.BMJ neurology open · 2021Article
- A ß-Secretase Modulator Decreases Tau Pathology and Preserves Short-Term Memory in a Mouse Model of Neurofibrillary Degeneration.Frontiers in pharmacology · 2021Article
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major goal in diseases is identifying a potential therapeutic agent that is cost-effective and can remedy some, if not all, disease symptoms. In Alzheimer's disease (AD), aggregation of hyperphosphorylated tau protein is one of the neuropathological hallmarks, and Tau pathology correlates better with cognitive impairments in AD patients than amyloid-β load, supporting a key role of tau-related mechanisms. Selenium is a non-metallic trace element that is incorporated in the brain into selenoproteins. Chronic treatment with sodium selenate, a non-toxic selenium compound, was recently reported to rescue behavioral phenotypes in tau mouse models. Here, we focused on the effects of chronic selenate application on synaptic transmission and synaptic plasticity in THY-Tau22 mice, a transgenic animal model of tauopathies. Three months with a supplement of sodium selenate in the drinking water (12 μg/ml) restored not only impaired neurocognitive functions but also rescued long-term depression (LTD), a major form of synaptic plasticity. Furthermore, selenate reduced the inactive demethylated catalytic subunit of protein phosphatase 2A (PP2A) in THY-Tau22 without affecting total PP2A.Our study provides evidence that chronic dietary selenate rescues functional synaptic deficits of tauopathy and identifies activation of PP2A as the putative mechanism.
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