ArticleCell communication and signaling : CCS2025
Caffeine mitigates ROS accumulation and attenuates motor neuron degeneration in the wobbler mouse model of amyotrophic lateral sclerosis.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- From animal models to metabolic interventions: Lessons from the Wobbler mouse.Neural regeneration research · 2026Article
- Antioxidant Supplementation with Caffeine During Rescue In Vitro Maturation Improves Fertilization and Embryo Development in Women of Advanced Maternal Age.Antioxidants (Basel, Switzerland) · 2026Article
- Polyphenolic Profile and Antioxidant Capacity of Coffee Silverskin Extracts: Insights from HPLC and GC-MS Analyses and Protective Effect in Schwann-like Cells.Antioxidants (Basel, Switzerland) · 2026Article
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Authors and funding
5 authors.
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Abstract
backgroundAmyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by oxidative stress and progressive motor neuron degeneration. This study evaluates the potential neuroprotective effects of caffeine in the Wobbler mouse, an established model of ALS.
methodsWobbler mice received caffeine supplementation (60 mg/kg/day) via drinking water, and key parameters, including muscle strength, NAD metabolism, oxidative stress, and motor neuron morphology, were assessed at critical disease stages.
resultsCaffeine delayed motor performance decline, as observed in grip strength tests during the early symptomatic phase. Histological analyses revealed that significantly fewer motor neurons were lost in caffeine-treated mice at p41, despite no changes in soma morphology. Biochemical assays demonstrated that caffeine significantly reduced ROS levels and restored NAD levels to wildtype-like values, although NMNAT2 protein expression remained unaffected. The data suggest that caffeine mitigates oxidative stress through alternative pathways, potentially involving enhanced mitochondrial function and antioxidative defenses.
conclusionsThese findings highlight the potential of caffeine as a protective agent for delaying motor neuron degeneration in ALS. Future studies should explore optimal dosing strategies, combinatorial treatment approaches, and the underlying molecular mechanisms, to enable translation of these findings to human ALS patients.
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