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Methylation of alpha-synuclein in a Sudanese cohort

dc.rights.licenseopenen_US
dc.contributor.authorBAKHIT, Yousuf
dc.contributor.authorSCHMITT, Ina
dc.contributor.authorHAMED, Ahlam
dc.contributor.authorIBRAHIM, Etedal Ahmed A.
dc.contributor.authorMOHAMED, Inaam N.
dc.contributor.authorEL-SADIG, Sarah M.
dc.contributor.authorELSEED, Maha A.
dc.contributor.authorALEBEED, Mohamed A.
dc.contributor.authorSHAHEEN, Mutaz T.
dc.contributor.authorIBRAHIM, Mohamed O.
dc.contributor.authorELHASSAN, Ali A.
dc.contributor.authorELTOM, Khalid
dc.contributor.authorALI, Hiba A.
dc.contributor.authorIBRAHIM, Yousuf A.
dc.contributor.authorALMAK, Murad E.
dc.contributor.authorABUBAKER, Rayan
dc.contributor.authorAHMED, Mohamed Anwer
dc.contributor.authorABUGRAIN, Ahmed A.
dc.contributor.authorELRASHEED, Salma M.
dc.contributor.authorOMAR, Mawia A.
dc.contributor.authorALMAHAL, Mohamed A.
dc.contributor.authorMOHAMEDSHARIF, Abubaker A.
dc.contributor.authorTAHIR, Mohamed Y.
dc.contributor.authorMALIK, Sawazen M.
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorELDIRDIRI, Hazim S.
dc.contributor.authorKHIDIR, Reem J.
dc.contributor.authorMOHAMED, Malaz T.
dc.contributor.authorABDALLA, Abdelmohaymin
dc.contributor.authorOMER, Farouk Yassen
dc.contributor.authorELSAYED, Liena E.O.
dc.contributor.authorBABIKIR, Haydar El Hadi
dc.contributor.authorBUKHARI, Elfateh Abd-Allah
dc.contributor.authorSEIDI, Osheik
dc.contributor.authorWÜLLNER, Ullrich
dc.date.accessioned2023-04-06T15:33:08Z
dc.date.available2023-04-06T15:33:08Z
dc.date.issued2022-08
dc.identifier.issn1353-8020en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/172860
dc.description.abstractEnBackground: Several studies suggested a significant role of epigenetic changes, including alterations in miRNA, histone modifications, and DNA methylation of α-synuclein (SNCA) in Parkinson’s disease (PD) pathogenicity. As of yet, only very few studies have been carried out in this field in Africa and none in Sudan. Materials and methods: We collected DNA from 172 Sudanese individuals (90 cases, 82 controls) who donated saliva for DNA extraction (mean age of onset: 40.6 ± 22.4 years). A family history of PD was evident in 64 patients. DNA preparation and bisulfite sequencing of SNCAintron1 was performed as described earlier. Results: Of the fourteen analyzed CpGs of SNCAintron1, CpGs 16-23 were hypomethylated in PD (P-value ranged from 0.023 to 0.003). P–values improved, when sporadic cases were excluded from the analysis. Conclusion: We identified the presence of a specific pattern of DNA methylation in a young Sudanese cohort of familial PD, which confirms the importance of the methylation of SNCAintron1 for PD. This phenomenon appears to be independent of ethnicity, the impact of environmental factors, drug history, or familial clustering.
dc.language.isoENen_US
dc.subject.enParkinson’s disease
dc.subject.enMethylation
dc.subject.enSudan
dc.subject.enSNCA
dc.title.enMethylation of alpha-synuclein in a Sudanese cohort
dc.title.alternativeParkinsonism Relat Disorden_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.parkreldis.2022.05.009en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed35728367en_US
bordeaux.journalParkinsonism and Related Disordersen_US
bordeaux.page6-8en_US
bordeaux.volume101en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamCircuits Neuronaux de l'Anxiétéen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04061376
hal.version1
hal.date.transferred2023-04-06T15:33:53Z
hal.exporttrue
dc.rights.ccPas de Licence CCen_US
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