The effects of lack of melatonin in experimental rat model of Alzheimer’s Disease: relationship with FEZ1 gene expression

dc.contributor.authorDemir, Mehmet
dc.contributor.authorYılmaz, Ümit
dc.contributor.authorÇolak, Cemil
dc.contributor.authorÇiğremiş, Yılmaz
dc.contributor.authorÖzyalın, Fatma
dc.contributor.authorTekedereli, İbrahim
dc.date.accessioned2021-11-23T12:10:19Z
dc.date.available2021-11-23T12:10:19Z
dc.date.issued2017
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAbstract: Alzheimer’s Disease (AD), which is the most common reason for dementia, is an irreversible neurodegenerative brain disease. FEZ1 is a protein expressed in the brain. High expressions of FEZ1 mRNA have been interpreted as an indicator of high neural plasticity for memory and learning. This study was planned to determine the effect of melatonin deficiency (pinealectomy; PnX) on AD and to reveal its association with FEZ1. 30 male rats were used in the study. The rats were divided into three as SHAM, PnX+streptozotocin (STZ) and PnX+STZ+melatonin (MLT) groups. The pineal glands of rats were surgically removed (except SHAM group) and STZ was intracerebroventricularly (icv) administrated at the first and third days. MLT (10 mg/kg/day) was intraperitoneally (ip) injected 1 h before the first STZ application and it was continued for 14 days. STZ and MLT solvents were applied to the rats in the SHAM group. At the end of the applications, Morris water maze (MWM) test was carried out the rats. At the end of MWM tests, the rats were sacrificed and their blood and hippocampus tissues were taken. FEZ1 gene expression and protein levels were determined from hippocampus tissue, while serum nonadrenaline, dopamine and serotonin levels were detected from blood samples. FEZ1 protein levels of PnX+STZ+MLT group were found to be statistically significantly lower than those of SHAM and PnX+STZ groups (p<0.05). While noradrenaline levels were found to be lower in both groups when compared with the SHAM group (p<0.05), no difference was found between the dopamine and serotonin levels of groups. Our results showed that in AD made up in the deficiency of melatonin, FEZ1 levels got higher and the increases were revealed to return to normal levels with exogenous melatonin applicationen_US
dc.identifier.citationDEMİR M,YILMAZ Ü,ÇOLAK C,ÇİĞREMİŞ Y,ÖZYALIN F,TEKEDERELİ İ,KILINÇLI A,SANDAL S (2017). The effects of lack of melatonin in experimental rat model of Alzheimer’s Disease: relationship with FEZ1 gene expression. Medicine Science, 6(2), 217 - 223.en_US
dc.identifier.endpage223en_US
dc.identifier.issn2147-0634
dc.identifier.issue2en_US
dc.identifier.startpage217en_US
dc.identifier.trdizinid263111en_US
dc.identifier.urihttps://hdl.handle.net/11616/43284
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/263111
dc.identifier.volume6en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofMedicine Scienceen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleThe effects of lack of melatonin in experimental rat model of Alzheimer’s Disease: relationship with FEZ1 gene expressionen_US
dc.typeArticleen_US

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