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dc.creatorArseniou S., Siokas V., Aloizou A.-M., Stamati P., Mentis A.-F.A., Tsouris Z., Dastamani M., Peristeri E., Valotassiou V., Bogdanos D.P., Hadjigeorgiou G.M., Dardiotis E.en
dc.date.accessioned2023-01-31T07:33:14Z
dc.date.available2023-01-31T07:33:14Z
dc.date.issued2020
dc.identifier10.1080/01616412.2020.1786973
dc.identifier.issn01616412
dc.identifier.urihttp://hdl.handle.net/11615/70817
dc.description.abstractBackground: Many studies support the hypothesis that brain glucose dysregulation contributes to neurodegeneration and disease progression. The SLC2A3 gene encodes the Neuronal Glucose Transporter 3 (GLUT3), a critical molecule for glucose transport into the neuron. The GLUT3 rs12842 polymorphism has been associated with an increased risk for attention-deficit/hyperactivity disorder (ADHD). Epidemiological and genetic studies have reported a link between antecedent ADHD and Alzheimer’s disease (AD), as both share a dysregulation of brain glucose. Aim: This study aimed to explore the possible correlation of the SLC2A3 rs12842 polymorphism with susceptibility towards AD. Methods: We genotyped 327 patients with AD and 327 controls for the GLUT3 rs12842. Results: Rs12842 was associated with a decreased risk of developing AD in the co-dominant [Odds Ratio (OR) (95% confidence interval (CI) = 0.67 (0.45–0.99)), p = 0.039], dominant [OR (95% CI) = 0.64 (0.44–0.93), p = 0.019] and log-additive modes [OR (95% CI) = 0.65 (0.46–0.91), p = 0.012]. Conclusions: Our results suggest a significant, inverse association between SLC2A3 rs12842 and the risk of AD. © 2020, © 2020 Informa UK Limited, trading as Taylor & Francis Group.en
dc.language.isoenen
dc.sourceNeurological Researchen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85087756777&doi=10.1080%2f01616412.2020.1786973&partnerID=40&md5=7ab9b2eca169c55fcbab23a908278700
dc.subjectgenomic DNAen
dc.subjectglucose transporter 3en
dc.subjectmicroRNAen
dc.subjecttau proteinen
dc.subjectglucose transporter 3en
dc.subjectSLC2A3 protein, humanen
dc.subjectageden
dc.subjectAlzheimer diseaseen
dc.subjectArticleen
dc.subjectattention deficit disorderen
dc.subjectautismen
dc.subjectbrain perfusionen
dc.subjectcase control studyen
dc.subjectcognitionen
dc.subjectdepressionen
dc.subjectdisease exacerbationen
dc.subjectDNA isolationen
dc.subjectDSM-IVen
dc.subjectexecutive functionen
dc.subjectfemaleen
dc.subjectgeneen
dc.subjectgene frequencyen
dc.subjectgenetic polymorphismen
dc.subjectgenetic risken
dc.subjectgenotypeen
dc.subjecthippocampusen
dc.subjecthumanen
dc.subjectmajor clinical studyen
dc.subjectmaleen
dc.subjectMini Mental State Examinationen
dc.subjectnuclear magnetic resonance imagingen
dc.subjectprevalenceen
dc.subjectrisk factoren
dc.subjectSanger sequencingen
dc.subjectsingle nucleotide polymorphismen
dc.subjectsingle photon emission computed tomographyen
dc.subjectAlzheimer diseaseen
dc.subjectgenetic predispositionen
dc.subjectgeneticsen
dc.subjectodds ratioen
dc.subjectsingle nucleotide polymorphismen
dc.subjectvery elderlyen
dc.subjectAgeden
dc.subjectAged, 80 and overen
dc.subjectAlzheimer Diseaseen
dc.subjectCase-Control Studiesen
dc.subjectFemaleen
dc.subjectGene Frequencyen
dc.subjectGenetic Predisposition to Diseaseen
dc.subjectGenotypeen
dc.subjectGlucose Transporter Type 3en
dc.subjectHumansen
dc.subjectMaleen
dc.subjectOdds Ratioen
dc.subjectPolymorphism, Single Nucleotideen
dc.subjectTaylor and Francis Ltd.en
dc.titleSLC2A3 rs12842 polymorphism and risk for Alzheimer’s diseaseen
dc.typejournalArticleen


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