ArticleInternational journal of molecular sciences2023
Spermidine Rescues Bioenergetic and Mitophagy Deficits Induced by Disease-Associated Tau Protein.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Mechanistic pathways linking gut microbial metabolites, microbial structural products, and host-microbe co-metabolites to mitochondrial function.Gut microbes · 2026Pooled it
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Mitochondrial quality control in human ageing and longevity.Nature metabolism · 2026Review
- Protocol for automated quantification of neuronal cells using the Agilent BioTek Cytation system and Gen5 neurite outgrowth module.STAR protocols · 2026Article
- LLPS Inflammasome Metabo-Proteostatic Failure Axis in AD: Mechanistic and Translational Insights.Molecular neurobiology · 2026Review
- Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.Cells · 2026Review
- Spermidine in the aging brain: mechanisms, preclinical evidence, and clinical perspectives.Molecular biology reports · 2026Review
- Article
- Platelet Autophagy as a Druggable Intracellular Pathway: Therapeutic Opportunities in Thromboinflammatory Diseases.Pharmaceutics · 2026Review
- Oral Supplementation With a Bovine Thymus Extract Reduces Neuronal Excitability in Aging Mice.FASEB bioAdvances · 2026Article
- Spermidine in Alzheimer's Disease: Evidence from Animal Models and Human Studies.Degenerative neurological and neuromuscular disease · 2026Review
- Mitochondrial Transplantation Increases Bioenergetics and Neurite Outgrowth in Healthy and P301Ltau-Expressing SH-SY5Y Cells.Molecular neurobiology · 2025Article
- Genetic factors and comorbid pathologies interact to drive regional mitophagy alterations in Lewy body dementia.Acta neuropathologica · 2025Article
- Management and Prevention of Neurodegenerative Disorders: Can Antioxidant-Rich Dietary Interventions Help?Antioxidants (Basel, Switzerland) · 2025Review
- Alterations and mechanistic insights of gut microbiota and its metabolites in type 2 diabetes mellitus and Alzheimer's disease.iMetaOmics · 2025Review
- Hippocampal mitophagy alterations in MAPT-associated frontotemporal dementia with parkinsonism.Acta neuropathologica communications · 2025Article
- Putrescine Depletion inPathogens (Basel, Switzerland) · 2025Article
- Targeting SMOX Preserves Optic Nerve Myelin, Axonal Integrity, and Visual Function in Multiple Sclerosis.Biomolecules · 2025Article
- Spermidine Enhances Mitochondrial Bioenergetics in Young and Aged Human-Induced Pluripotent Stem Cell-Derived Neurons.Antioxidants (Basel, Switzerland) · 2024Article
- Human iPSCs from Aged Donors Retain Their Mitochondrial Aging Signature.International journal of molecular sciences · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal tau build-up is a hallmark of Alzheimer's disease (AD) and more than 20 other serious neurodegenerative diseases. Mitochondria are paramount organelles playing a predominant role in cellular bioenergetics, namely by providing the main source of cellular energy via adenosine triphosphate generation. Abnormal tau impairs almost every aspect of mitochondrial function, from mitochondrial respiration to mitophagy. The aim of our study was to investigate the effects of spermidine, a polyamine which exerts neuroprotective effects, on mitochondrial function in a cellular model of tauopathy. Recent evidence identified autophagy as the main mechanism of action of spermidine on life-span prolongation and neuroprotection, but the effects of spermidine on abnormal tau-induced mitochondrial dysfunction have not yet been investigated. We used SH-SY5Y cells stably expressing a mutant form of human tau protein (P301L tau mutation) or cells expressing the empty vector (control cells). We showed that spermidine improved mitochondrial respiration, mitochondrial membrane potential as well as adenosine triphosphate (ATP) production in both control and P301L tau-expressing cells. We also showed that spermidine decreased the level of free radicals, increased autophagy and restored P301L tau-induced impairments in mitophagy. Overall, our findings suggest that spermidine supplementation might represent an attractive therapeutic approach to prevent/counteract tau-related mitochondrial impairments.
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Registered trials
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