ArticlePloS one2013
Vitamin D(3) at 50x AI attenuates the decline in paw grip endurance, but not disease outcomes, in the G93A mouse model of ALS, and is toxic in females.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.
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Who cites it
22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 36 citations in OpenAlex.
- Is There a Role for Vitamin D in Amyotrophic Lateral Sclerosis? A Systematic Review and Meta-Analysis.Frontiers in neurology · 2020Pooled it
- State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model.Amyotrophic lateral sclerosis & frontotemporal degeneration · 2015Pooled it
- Characterization of the Contribution of Genetic Background and Gender to Disease Progression in the SOD1 G93A Mouse Model of Amyotrophic Lateral Sclerosis: A Meta-Analysis.Journal of neuromuscular diseasesPooled it
- Vitamin D and Neurodegenerative Diseases Such as Multiple Sclerosis (MS), Parkinson's Disease (PD), Alzheimer's Disease (AD), and Amyotrophic Lateral Sclerosis (ALS): A Review of Current Literature.Current nutrition reports · 2025Review
- Unlocking the Potential of Vitamin D: A Comprehensive Exploration of Its Role in Neurological Health and Diseases.Biology · 2025Review
- Exploration of the Role of Vitamins in Preventing Neurodegenerative Diseases: Comprehensive Review on Preclinical and Clinical Findings.Current neuropharmacology · 2025Review
- Vitamin D in Central Nervous System: Implications for Neurological Disorders.International journal of molecular sciences · 2024Review
- The Role of Vitamins in Neurodegenerative Disease: An Update.Biomedicines · 2021Review
- The Role of the Microbiota-Gut-Brain Axis and Antibiotics in ALS and Neurodegenerative Diseases.Microorganisms · 2020Review
- Maximizing the Survival of Amyotrophic Lateral Sclerosis Patients: Current Perspectives.Neurology research international · 2018Review
- Vitamin D and Neurological Diseases: An Endocrine View.International journal of molecular sciences · 2017Review
- Exploring targets and therapies for amyotrophic lateral sclerosis: current insights into dietary interventions.Degenerative neurological and neuromuscular disease · 2017Review
- Palliative Care Issues in Amyotrophic Lateral Sclerosis: An Evidenced-Based Review.The American journal of hospice & palliative care · 2016Review
- Current Therapy of Drugs in Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2016Review
- Screening of Drugs Inhibiting In vitro Oligomerization of Cu/Zn-Superoxide Dismutase with a Mutation Causing Amyotrophic Lateral Sclerosis.Frontiers in molecular biosciences · 2016Article
- Complementary and Alternative Therapies in Amyotrophic Lateral Sclerosis.Neurologic clinics · 2015Review
- Vitamin D is Not a Protective Factor in ALS.CNS neuroscience & therapeutics · 2015Article
- Article
- Vitamin D as a potential therapy in amyotrophic lateral sclerosis.CNS neuroscience & therapeutics · 2014Review
- Dietary vitamin D3 supplementation at 10× the adequate intake improves functional capacity in the G93A transgenic mouse model of ALS, a pilot study.CNS neuroscience & therapeutics · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe previously demonstrated that dietary vitamin D(3) at 10x the adequate intake (AI) attenuates the decline in functional capacity in the G93A mouse model of ALS. We hypothesized that higher doses would elicit more robust changes in functional and disease outcomes.
objectiveTo determine the effects of dietary vitamin D(3) at 50xAI on functional outcomes (motor performance, paw grip endurance) and disease severity (clinical score), as well as disease onset, disease progression and lifespan in the transgenic G93A mouse model of ALS.
methodsStarting at age 25 d, 100 G93A mice (55 M, 45 F) were provided ad libitum with either an adequate (AI; 1 IU D(3)/g feed) or high (HiD; 50 IU D(3)/g feed) vitamin D(3) diet.
resultsHiD females consumed 9% less food corrected for body weight vs. AI females (P = 0.010). HiD mice had a 12% greater paw grip endurance over time between age 60-141 d (P = 0.015), and a 37% greater score during disease progression (P = 0.042) vs. AI mice. Although HiD females had a non-significant 31% greater CS prior to disease onset vs. AI females, they exhibited a significant 20% greater paw grip endurance AUC (P = 0.020) when corrected for clinical score.
conclusionDietary D(3) supplementation at 50x the adequate intake attenuated the decline in paw grip endurance, but did not influence age at disease onset, hindlimb paralysis or endpoint in the transgenic G93A mouse model of ALS. Furthermore, females may have reached the threshold for vitamin D(3) toxicity as evidence by reduced food intake and greater disease severity prior to disease onset.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.