Neonatal neurodegeneration in alzheimer's disease transgenic mouse model

dc.authorid0000-0002-1079-8832
dc.contributor.authorMazi, Aişe Rümeysa
dc.contributor.authorArzuman, Ayşegül Sümeyye
dc.contributor.authorGürel, Büşra
dc.contributor.authorŞahin, Betül
dc.contributor.authorTüzüner, Mete Bora
dc.contributor.authorOzansoy, Mehmet
dc.contributor.authorBaykal, Ahmet Tarık
dc.date.accessioned2021-01-27T06:56:02Z
dc.date.available2021-01-27T06:56:02Z
dc.date.issued2018
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalı
dc.description.abstractAlzheimer's disease (AD) is a progressive disorder characterized by a variety of molecular pathologies causing cortical dementia with a prominent memory deficit. Formation of the pathology, which begins decades before the diagnosis of the disease, is highly correlated with the clinical symptoms. Several proteomics studies were performed using animal models to monitor the alterations of the brain tissue proteome at different stages of AD. However, proteome changes in the brain regions of newborn transgenic mouse model have not been investigated yet. To this end, we analyzed protein expression alterations in cortex, hippocampus and cerebellum of transgenic mice carrying five familial AD mutations (5XFAD) at neonatal day-1. Our results indicate a remarkable difference in protein expression profile of newborn 5XFAD brain with region specific variations. Additionally, the proteins, which show similar expression alteration pattern in postmortem human AD brains, were determined. Bioinformatics analysis showed that the molecular alterations were mostly related to the cell morphology, cellular assembly and organization, and neuroinflammation. Moreover, morphological analysis revealed that there is an increase in neurite number of 5XFAD mouse neurons in vitro. We suggest that, molecular alterations in the AD brain exist even at birth, and perhaps the disease is silenced until older ages when the brain becomes vulnerable.
dc.identifier.citationMazi, A. R., Arzuman, A. S., Gürel, B., Şahin, B., Tüzüner, M. B., Ozansoy, M. ... Baykal, A. T. (2018). Neonatal neurodegeneration in alzheimer's disease transgenic mouse model. IOS Press, 2(1), 79-91. https://dx.doi.org/10.3233/ADR-170049
dc.identifier.doi10.3233/ADR-170049
dc.identifier.endpage91
dc.identifier.issn2542-4823
dc.identifier.issue1
dc.identifier.startpage79
dc.identifier.urihttps://dx.doi.org/10.3233/ADR-170049
dc.identifier.urihttps://hdl.handle.net/20.500.12511/6406
dc.identifier.volume2
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherIOS Press
dc.relation.ispartofJournal of Alzheimer's Disease Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsAttribution-NonCommercial 4.0 International*
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/legalcode*
dc.subjectAlzheimer’s Disease
dc.subjectCerebellum
dc.subjectCortex
dc.subjectHippocampus
dc.subjectNeonatal Neurodegeneration
dc.subjectProteomics
dc.titleNeonatal neurodegeneration in alzheimer's disease transgenic mouse model
dc.typeArticle

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