ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Selenomethionine Mitigates Cognitive Decline by Targeting Both Tau Hyperphosphorylation and Autophagic Clearance in an Alzheimer's Disease Mouse Model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- Gut microbiota in patients with Alzheimer's disease spectrum: a systematic review and meta-analysis.Aging · 2022Pooled it
- SRSF1 as a promising biomarker and key player in the pathogenesis of Alzheimer's disease.Molecular medicine reports · 2026Article
- Selenium and resveratrol attenuate rotenone-induced Parkinson's disease in zebrafish model.Molecular biology reports · 2025Article
- Exploring the Neuroprotective Role of Selenium: Implications and Perspectives for Central Nervous System Disorders.Exploration (Beijing, China) · 2025Review
- Selenoprotein K Confers Protection against Iron Dyshomeostasis-Related Neurotoxicity by Regulating the Palmitoylation of TfR-1.Journal of agricultural and food chemistry · 2025Article
- 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
- Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model.Communications biology · 2024Article
- Evaluation of the Neuroprotective Effect of Organic Selenium Compounds: An in Vitro Model of Alzheimer's Disease.Biological trace element research · 2024Article
- Evaluation of the Neuroprotective Effect of Organic Selenium Compounds: An in Vitro Model of Alzheimer's Disease.Biological trace element research · 2024Article
- Autophagy-modulating biomaterials: multifunctional weapons to promote tissue regeneration.Cell communication and signaling : CCS · 2024Review
- Ebselen: A Review on its Synthesis, Derivatives, Anticancer Efficacy and Utility in Combating SARS-COV-2.Mini reviews in medicinal chemistry · 2024Review
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Memory Recovery Effect of a New Bioactive Innovative Combination in Rats with Experimental Dementia.Antioxidants (Basel, Switzerland) · 2023Article
- Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023Review
- Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System.Biomolecules · 2023Review
- Different Effects and Mechanisms of Selenium Compounds in Improving Pathology in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- Non-Enzymatic Antioxidants against Alzheimer's Disease: Prevention, Diagnosis and Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- The Metabolic Basis for Nervous System Dysfunction in Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease.Current neurovascular research · 2023Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tau pathology was recently identified as a key driver of disease progression and an attractive therapeutic target in Alzheimer's disease (AD). Selenomethionine (Se-Met), a major bioactive form of selenium (Se) in organisms with significant antioxidant capacity, reduced the levels of total tau and hyperphosphorylated tau and ameliorated cognitive deficits in younger triple transgenic AD (3xTg-AD) mice. Whether Se-Met has a similar effect on tau pathology and the specific mechanism of action in older 3xTg-AD mice remains unknown. Autophagy is a major self-degradative process to maintain cellular homeostasis and function. Autophagic dysfunction has been implicated in the pathogenesis of multiple age-dependent diseases, including AD. Modulation of autophagy has been shown to retard the accumulation of misfolded and aggregated proteins and to delay the progression of AD. Here, we found that 3xTg-AD mice showed significant improvement in cognitive ability after a 3-month treatment with Se-Met beginning at 8 months of age. In addition to attenuating the hyperphosphorylation of tau by modulating the activity of Akt/glycogen synthase kinase-3β and protein phosphatase 2A, Se-Met-induced reduction of tau was also mediated by an autophagy-based pathway. Specifically, Se-Met improved the initiation of autophagy via the AMP-activated protein kinase-mTOR (mammalian target of rapamycin) signaling pathway and enhanced autophagic flux to promote the clearance of tau in 3xTg-AD mice and primary 3xTg neurons. Thus, our results demonstrate for the first time that Se-Met mitigates cognitive decline by targeting both the hyperphosphorylation of tau and the autophagic clearance of tau in AD mice. These data strongly support Se-Met as a potent nutraceutical for AD therapy.
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Registered trials
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