P. Longone, A. Davoli, V. Greco, A. Spalloni, E. Guatteo, C. Nerí, Giada Ricciardo Rizzo, Alberto Cordella, A. Romigi, C. Cortese, S. Bernardini, P. Sarchielli, G. Cardaioli, P. Calabresi, A. Urbani, N. Mercuri
{"title":"Hydrogen sulphide \"a double-faced Janus\" in amyotrophic lateral sclerosis (ALS)","authors":"P. Longone, A. Davoli, V. Greco, A. Spalloni, E. Guatteo, C. Nerí, Giada Ricciardo Rizzo, Alberto Cordella, A. Romigi, C. Cortese, S. Bernardini, P. Sarchielli, G. Cardaioli, P. Calabresi, A. Urbani, N. Mercuri","doi":"10.14800/TTND.749","DOIUrl":null,"url":null,"abstract":"We have recently published a paper in Annals of Neurology entitled “Evidence of Hydrogen Sulphide involvement in Amyotrophic Lateral Sclerosis” [1] where we reported a study performed in patients, and in a genetic model of familial ALS. The outcome of this study is an original finding: the overproduction of hydrogen sulphide (H 2 S) in the human patients and in the animal model. We also show that H 2 S is produced, mainly, by glial cells, is toxic to motor neurons and increases significantly cytosolic Ca 2+ concentration. Altogether, our data introduce H 2 S as a new contestant in the ALS-related toxic pathways, which has potential implications for innovative drug design in ALS.","PeriodicalId":90750,"journal":{"name":"Therapeutic targets for neurological diseases","volume":"2 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2015-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Therapeutic targets for neurological diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14800/TTND.749","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3
Abstract
We have recently published a paper in Annals of Neurology entitled “Evidence of Hydrogen Sulphide involvement in Amyotrophic Lateral Sclerosis” [1] where we reported a study performed in patients, and in a genetic model of familial ALS. The outcome of this study is an original finding: the overproduction of hydrogen sulphide (H 2 S) in the human patients and in the animal model. We also show that H 2 S is produced, mainly, by glial cells, is toxic to motor neurons and increases significantly cytosolic Ca 2+ concentration. Altogether, our data introduce H 2 S as a new contestant in the ALS-related toxic pathways, which has potential implications for innovative drug design in ALS.
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