{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gonzalez Cardona J"],"funding":["National Institute of Neurological Disorders and Stroke","Medimmune","NINDS NIH HHS","NIGMS NIH HHS"],"pagination":["e0221747"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6730995"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["Multiple sclerosis (MS) is characterized by demyelinated lesions in the central nervous system. Destruction of myelin and secondary damage to axons and neurons leads to significant disability, particularly in people with progressive MS. Accumulating evidence suggests that the potential for myelin repair exists in MS, although for unclear reasons this process fails. The cells responsible for producing myelin, the oligodendrocytes, and their progenitors, oligodendrocyte precursor cells (OPCs), have been identified at the site of lesions, even in adults. Their presence suggests the possibility that endogenous remyelination without transplantation of donor stem cells may be a mechanism for myelin repair in MS. Strategies to develop novel therapies have focused on induction of signaling pathway"],"journal":["PloS one"],"pubmed_title":["Quetiapine has an additive effect to triiodothyronine in inducing differentiation of oligodendrocyte precursor cells through induction of cholesterol biosynthesis."],"pmcid":["PMC6730995"],"funding_grant_id":["R37 NS041435","NS050274","T32 GM008752","R37NS041435","P30 NS050274"],"pubmed_authors":["Whartenby KA","Gonzalez Cardona J","Kirby L","Davidson T","Smith MD","Wang J","Schott JT","Karnell JL","Calabresi PA"],"additional_accession":[]},"is_claimable":false,"name":"Quetiapine has an additive effect to triiodothyronine in inducing differentiation of oligodendrocyte precursor cells through induction of cholesterol biosynthesis.","description":"Multiple sclerosis (MS) is characterized by demyelinated lesions in the central nervous system. Destruction of myelin and secondary damage to axons and neurons leads to significant disability, particularly in people with progressive MS. Accumulating evidence suggests that the potential for myelin repair exists in MS, although for unclear reasons this process fails. The cells responsible for producing myelin, the oligodendrocytes, and their progenitors, oligodendrocyte precursor cells (OPCs), have been identified at the site of lesions, even in adults. Their presence suggests the possibility that endogenous remyelination without transplantation of donor stem cells may be a mechanism for myelin repair in MS. Strategies to develop novel therapies have focused on induction of signaling pathway","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019","modification":"2025-04-04T10:33:13.747Z","creation":"2019-09-24T07:08:31Z"},"accession":"S-EPMC6730995","cross_references":{"pubmed":["31490950"],"doi":["10.1371/journal.pone.0221747"]}}