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Decreased plasma agmatine levels in autistic subjects

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dc.contributor.author Esnafoglu, Erman
dc.contributor.author Irende, Ilhan
dc.date.accessioned 2022-08-17T05:26:02Z
dc.date.available 2022-08-17T05:26:02Z
dc.date.issued 2018
dc.identifier.uri http://doi.org/10.1007/s00702-017-1836-2
dc.identifier.uri http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/2278
dc.description.abstract Agmatine is a polyamine endogenously synthesized from arginine and is considered to be a new neurotransmitter. Agmatine has been implicated in the pathophysiology of several diseases such as anxiety disorder, depression, and schizophrenia. Agmatine also possesses anticonvulsant, neuroprotective, antiapoptotic, antioxidant, anxiolytic, and antidepressant effects. Furthermore, agmatine inhibits the nitric oxide synthase enzyme and exerts antagonist effects on NMDA, alpha-2, and imidazoline receptors. Considering these characteristics, the present study investigated whether agmatine plays a role in the pathogenesis of autistic spectrum disorders (ASDs). Therefore, plasma agmatine levels were evaluated in 34 patients with ASD and 28 non-ASD controls. Plasma agmatine levels were measured using the HPLC method. The study found remarkably lower agmatine levels in patients with ASD compared with the non-ASD control group (p < 0.001). These findings support the notion that agmatine might contribute to the pathogenesis of ASD and may serve as a new target for treatment. en_US
dc.language.iso eng en_US
dc.publisher SPRINGER WIEN, SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA en_US
dc.relation.isversionof 10.1007/s00702-017-1836-2 en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.subject Autism spectrum disorder; Autism; Agmatine; Polyamines; Pathogenesis; NMDA receptors en_US
dc.title Decreased plasma agmatine levels in autistic subjects en_US
dc.type article en_US
dc.relation.journal JOURNAL OF NEURAL TRANSMISSION en_US
dc.contributor.department Ordu Üniversitesi en_US
dc.contributor.authorID 0000-0001-8685-1153 en_US
dc.identifier.volume 125 en_US
dc.identifier.issue 4 en_US
dc.identifier.startpage 735 en_US
dc.identifier.endpage 740 en_US


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