Literature DB >> 31197218

Vitamin D supplementation has no effects on progression of motor dysfunction in amyotrophic lateral sclerosis (ALS).

Francesca Trojsi1, Mattia Siciliano2,3, Carla Passaniti2,3, Alvino Bisecco2, Antonio Russo2, Luigi Lavorgna2, Sabrina Esposito2, Dario Ricciardi2, Maria Rosaria Monsurrò2, Gioacchino Tedeschi2, Gabriella Santangelo3.   

Abstract

OBJECTIVES: To investigate the effects of cholecalciferol supplementation on the progression of motor disability in a cohort of amyotrophic lateral sclerosis (ALS) patients with low blood 25-hydroxyvitamin D3 [25(OH)D] levels, on the basis of the hypothesis of potential neuroprotective effects of vitamin D supplementation.
METHODS: Forty-eight ALS patients, 34 with deficient (<20 ng/mL) and 14 with insufficient (20-29 ng/mL) serum levels of 25(OH)D, were randomized and treated by 3 different doses of cholecalciferol [50.000, 75.000 and 100.000 international units (IU) /month] and evaluated after 6-months. Assessment of motor dysfunction at baseline and after 6 months included ALS Functional Rating Scale-Revised (ALFRS-R) and upper motor neuron (UMN) scores and blood samples for 25(OH)D levels.
RESULTS: Clinical data of 33 patients were available after 6 months. Analysis of Covariance (ANCOVA), with pre-treatment measurements included as covariate, did not show statistically significant differences in the ALSFRS-R (p > 0.05) and UMN (p > 0.05) among the patient groups who underwent 3 different doses of cholecalciferol. Conversely, the treatment with 75.000 IU/month or 100.000 IU/month induced a significant increase in serum levels of 25(OH)D in comparison with the supplementation with 50.000 IU/month; no significant differences were found between 75.000 IU/month and 100.000 IU/month.
CONCLUSIONS: Our findings highlighted that 6-month supplementation of vitamin D in ALS patients had no significant effects on motor dysfunction. However, it is recommended to prevent medical complications of vitamin D deficiency in ALS patients as well as in other populations of neurodegenerative patients, characterized by low mobility and decreased sun exposure.

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Year:  2019        PMID: 31197218     DOI: 10.1038/s41430-019-0448-3

Source DB:  PubMed          Journal:  Eur J Clin Nutr        ISSN: 0954-3007            Impact factor:   4.016


  39 in total

1.  Dietary vitamin D3 supplementation at 10× the adequate intake improves functional capacity in the G93A transgenic mouse model of ALS, a pilot study.

Authors:  Alexandro Gianforcaro; Mazen J Hamadeh
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Review 2.  Vitamin D and the regulation of Wnt/beta-catenin signaling and innate immunity in colorectal cancer.

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Journal:  Nutr Rev       Date:  2007-08       Impact factor: 7.110

3.  1α,25-Dihydroxyvitamin D3 reduces cerebral amyloid-β accumulation and improves cognition in mouse models of Alzheimer's disease.

Authors:  Matthew R Durk; Kyung Han; Edwin C Y Chow; Rosemary Ahrens; Jeffrey T Henderson; Paul E Fraser; K Sandy Pang
Journal:  J Neurosci       Date:  2014-05-21       Impact factor: 6.167

4.  Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS.

Authors:  Anya M Y Lin; K B Chen; P L Chao
Journal:  Ann N Y Acad Sci       Date:  2005-08       Impact factor: 5.691

5.  1,25-dihydroxyvitamin D3 regulates the synthesis of gamma-glutamyl transpeptidase and glutathione levels in rat primary astrocytes.

Authors:  E Garcion; L Sindji; G Leblondel; P Brachet; F Darcy
Journal:  J Neurochem       Date:  1999-08       Impact factor: 5.372

6.  Progesterone with vitamin D affords better neuroprotection against excitotoxicity in cultured cortical neurons than progesterone alone.

Authors:  Fahim Atif; Iqbal Sayeed; Tauheed Ishrat; Donald G Stein
Journal:  Mol Med       Date:  2009-06-26       Impact factor: 6.354

7.  Vitamin D3 deficiency differentially affects functional and disease outcomes in the G93A mouse model of amyotrophic lateral sclerosis.

Authors:  Jesse A Solomon; Alexandro Gianforcaro; Mazen J Hamadeh
Journal:  PLoS One       Date:  2011-12-27       Impact factor: 3.240

8.  Dietary Vitamin D3 Restriction Exacerbates Disease Pathophysiology in the Spinal Cord of the G93A Mouse Model of Amyotrophic Lateral Sclerosis.

Authors:  Elnaz Moghimi; Jesse A Solomon; Alexandro Gianforcaro; Mazen J Hamadeh
Journal:  PLoS One       Date:  2015-05-28       Impact factor: 3.240

Review 9.  Vitamin D and Neurological Diseases: An Endocrine View.

Authors:  Carolina Di Somma; Elisabetta Scarano; Luigi Barrea; Volha V Zhukouskaya; Silvia Savastano; Chiara Mele; Massimo Scacchi; Gianluca Aimaretti; Annamaria Colao; Paolo Marzullo
Journal:  Int J Mol Sci       Date:  2017-11-21       Impact factor: 5.923

10.  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.

Authors:  Alexandro Gianforcaro; Jesse A Solomon; Mazen J Hamadeh
Journal:  PLoS One       Date:  2013-02-06       Impact factor: 3.240

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  5 in total

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Authors:  Chinnappa A Uthaiah; Narasimha M Beeraka; R Rajalakshmi; C M Ramya; SubbaRao V Madhunapantula
Journal:  Mol Neurobiol       Date:  2022-04-27       Impact factor: 5.590

Review 2.  Pathophysiology and Treatment of Non-motor Dysfunction in Amyotrophic Lateral Sclerosis.

Authors:  Colin J Mahoney; Rebekah M Ahmed; William Huynh; Sicong Tu; Jonathan D Rohrer; Richard S Bedlack; Orla Hardiman; Matthew C Kiernan
Journal:  CNS Drugs       Date:  2021-05-15       Impact factor: 5.749

Review 3.  Potential Preventive Strategies for Amyotrophic Lateral Sclerosis.

Authors:  B Kuraszkiewicz; H Goszczyńska; T Podsiadły-Marczykowska; M Piotrkiewicz; P Andersen; M Gromicho; J Grosskreutz; M Kuźma-Kozakiewicz; S Petri; B Stubbendorf; K Szacka; H Uysal; M de Carvalho
Journal:  Front Neurosci       Date:  2020-05-26       Impact factor: 4.677

4.  Use of Off-Label Drugs and Nutrition Supplements among Patients with Amyotrophic Lateral Sclerosis in Norway.

Authors:  Gard Aasmund Skulstad Johanson; Ole-Bjørn Tysnes; Tale L Bjerknes
Journal:  Neurol Res Int       Date:  2022-04-12

Review 5.  A chemogenomic approach is required for effective treatment of amyotrophic lateral sclerosis.

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Journal:  Clin Transl Med       Date:  2022-01
  5 in total

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