Vitamin D as a Potential Therapy in Amyotrophic Lateral Sclerosis
Identifieur interne : 000B80 ( Main/Exploration ); précédent : 000B79; suivant : 000B81Vitamin D as a Potential Therapy in Amyotrophic Lateral Sclerosis
Auteurs : Alexandro Gianforcaro [Canada] ; Mazen J. Hamadeh [Canada]Source :
- CNS neuroscience & therapeutics : (Print) [ 1755-5930 ] ; 2014.
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- Pascal (Inist)
English descriptors
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Abstract
Vitamin D has been demonstrated to influence multiple aspects of amyotrophic lateral sclerosis (ALS) pathology. Both human and rodent central nervous systems express the vitamin D receptor (VDR) and/or its enzymatic machinery needed to fully activate the hormone. Clinical research suggests that vitamin D treatment can improve compromised human muscular ability and increase muscle size, supported by loss of motor function and muscle mass in animals following VDR knockout, as well as increased muscle protein synthesis and ATP production following vitamin D supplementation. Vitamin D has also been shown to reduce the expression of biomarkers associated with oxidative stress and inflammation in patients with multiple sclerosis, rheumatoid arthritis, congestive heart failure, Parkinson's disease and Alzheimer's disease; diseases that share common pathophysiologies with ALS. Furthermore, vitamin D treatment greatly attenuates hypoxic brain damage in vivo and reduces neuronal lethality of glutamate insult in vitro; a hallmark trait of ALS glutamate excitotoxicity. We have recently shown that high-dose vitamin D3 supplementation improved, whereas vitamin D3 restriction worsened, functional capacity in the G93A mouse model of ALS. In sum, evidence demonstrates that vitamin D, unlike the antiglutamatergic agent Riluzole, affects multiple aspects of ALS pathophysiology and could provide a greater cumulative effect.
Affiliations:
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Hamadeh</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>School of Kinesiology and Health Science, Faculty of Health, and Muscle Health Research Centre, York University</s1><s2>Toronto, ON</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, ON</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">14-0078632</idno><date when="2014">2014</date><idno type="stanalyst">PASCAL 14-0078632 INIST</idno><idno type="RBID">Pascal:14-0078632</idno><idno type="wicri:Area/PascalFrancis/Corpus">000034</idno><idno type="wicri:Area/PascalFrancis/Curation">000B84</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000000</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000000</idno><idno type="wicri:doubleKey">1755-5930:2014:Gianforcaro A:vitamin:d:as</idno><idno type="wicri:Area/Main/Merge">000B85</idno><idno type="wicri:Area/Main/Curation">000B80</idno><idno type="wicri:Area/Main/Exploration">000B80</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Vitamin D as a Potential Therapy in Amyotrophic Lateral Sclerosis</title><author><name sortKey="Gianforcaro, Alexandro" sort="Gianforcaro, Alexandro" uniqKey="Gianforcaro A" first="Alexandro" last="Gianforcaro">Alexandro Gianforcaro</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>School of Kinesiology and Health Science, Faculty of Health, and Muscle Health Research Centre, York University</s1><s2>Toronto, ON</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, ON</wicri:noRegion></affiliation></author><author><name sortKey="Hamadeh, Mazen J" sort="Hamadeh, Mazen J" uniqKey="Hamadeh M" first="Mazen J." last="Hamadeh">Mazen J. Hamadeh</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>School of Kinesiology and Health Science, Faculty of Health, and Muscle Health Research Centre, York University</s1><s2>Toronto, ON</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto, ON</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">CNS neuroscience & therapeutics : (Print)</title><title level="j" type="abbreviated">CNS neurosci. ther. : (Print)</title><idno type="ISSN">1755-5930</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">CNS neuroscience & therapeutics : (Print)</title><title level="j" type="abbreviated">CNS neurosci. ther. : (Print)</title><idno type="ISSN">1755-5930</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amyotrophic lateral sclerosis</term><term>Animal</term><term>Apoptosis</term><term>Calcitriol</term><term>Cell death</term><term>Cholecalciferol(1,25-dihydroxy)</term><term>Excitotoxicity</term><term>Inflammation</term><term>Motor neuron</term><term>Mouse</term><term>Neuromuscular diseases</term><term>Oxidative stress</term><term>Treatment</term><term>Vitamin D</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Sclérose latérale amyotrophique</term><term>Pathologie neuromusculaire</term><term>Vitamine D</term><term>Traitement</term><term>Apoptose</term><term>Calcitriol</term><term>Cholécalciférol(1,25-dihydroxy)</term><term>Animal</term><term>Souris</term><term>Excitotoxicité</term><term>Inflammation</term><term>Neurone moteur</term><term>Mort cellulaire</term><term>Stress oxydatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vitamin D has been demonstrated to influence multiple aspects of amyotrophic lateral sclerosis (ALS) pathology. Both human and rodent central nervous systems express the vitamin D receptor (VDR) and/or its enzymatic machinery needed to fully activate the hormone. Clinical research suggests that vitamin D treatment can improve compromised human muscular ability and increase muscle size, supported by loss of motor function and muscle mass in animals following VDR knockout, as well as increased muscle protein synthesis and ATP production following vitamin D supplementation. Vitamin D has also been shown to reduce the expression of biomarkers associated with oxidative stress and inflammation in patients with multiple sclerosis, rheumatoid arthritis, congestive heart failure, Parkinson's disease and Alzheimer's disease; diseases that share common pathophysiologies with ALS. Furthermore, vitamin D treatment greatly attenuates hypoxic brain damage in vivo and reduces neuronal lethality of glutamate insult in vitro; a hallmark trait of ALS glutamate excitotoxicity. We have recently shown that high-dose vitamin D<sub>3</sub> supplementation improved, whereas vitamin D<sub>3</sub> restriction worsened, functional capacity in the G93A mouse model of ALS. In sum, evidence demonstrates that vitamin D, unlike the antiglutamatergic agent Riluzole, affects multiple aspects of ALS pathophysiology and could provide a greater cumulative effect.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Gianforcaro, Alexandro" sort="Gianforcaro, Alexandro" uniqKey="Gianforcaro A" first="Alexandro" last="Gianforcaro">Alexandro Gianforcaro</name></noRegion><name sortKey="Hamadeh, Mazen J" sort="Hamadeh, Mazen J" uniqKey="Hamadeh M" first="Mazen J." last="Hamadeh">Mazen J. Hamadeh</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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