The effects and interactions of APOE and APH-1A polymorphisms in Alzheimer disease

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dc.authoridKOC, EMINE RABIA/0000-0002-0264-7284|acar, muradiye/0000-0003-4357-5229;
dc.contributor.authorAcar Cinleti, Burcu
dc.contributor.authorYardimci, Nilgul
dc.contributor.authorAyturk, Zubeyde
dc.contributor.authorIlhan, Atilla
dc.contributor.authorKaya, Gulhan
dc.contributor.authorAcar, Muradiye
dc.contributor.authorKoc, Emine Rabia
dc.date.accessioned2025-10-24T18:09:56Z
dc.date.available2025-10-24T18:09:56Z
dc.date.issued2015
dc.departmentMalatya Turgut Özal Üniversitesi
dc.description.abstractBackground/aim: Alzheimer disease (AD) is characterized by the accumulation of senile plaques composed of amyloid beta-peptide, which is derived from beta-amyloid precursor protein through degradation by beta-secretase and.-secretase complexes. One of the major components of gamma-secretase complex, anterior pharynx-defective-1 (APH-1), is responsible for the activity of the.-secretase complex. In this study, we searched for not only the most known common genetic risk factor, APOE, but also the APH-1a gene polymorphism in AD patients in a Turkish population. Materials and methods: In this study, 49 AD patients and 45 healthy controls were included. The genetic polymorphisms and allele frequencies of APOE and APH-1a were investigated. Patients were evaluated for behavioral, cognitive, and functional domains by detailed neurocognitive tests, and comparison between the above-mentioned polymorphisms and disease severity was made. Results: Although there was an increased tendency of the APO epsilon 4 allele in the AD group, no statistically significant difference was detected either in APOE or APH-1a polymorphisms, not suggesting a strong susceptibility to the development of AD. Conclusion: While searching for the pathogenesis of AD in order to develop novel diagnostic as well as therapeutic approaches, analysis of other genes with a possible role in AD is warranted.
dc.description.sponsorshipScientific Research Fund of Turgut Ozal University [2013-04-002]
dc.description.sponsorshipThis work was supported by the Scientific Research Fund of Turgut Ozal University under project number 2013-04-002.
dc.identifier.doi10.3906/sag-1407-19
dc.identifier.endpage1105
dc.identifier.issn1300-0144
dc.identifier.issn1303-6165
dc.identifier.issue5
dc.identifier.pmid26738354
dc.identifier.scopus2-s2.0-84943242418
dc.identifier.scopusqualityQ1
dc.identifier.startpage1098
dc.identifier.trdizinid180118
dc.identifier.urihttps://doi.org/10.3906/sag-1407-19
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/180118
dc.identifier.urihttps://hdl.handle.net/20.500.12899/3879
dc.identifier.volume45
dc.identifier.wosWOS:000362526300019
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakTR-Dizin
dc.language.isoen
dc.publisherTubitak Scientific & Technological Research Council Turkey
dc.relation.ispartofTurkish Journal Of Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20251023
dc.subjectAlzheimer disease; APOE; APH-1A; polymorphism; biomarker
dc.titleThe effects and interactions of APOE and APH-1A polymorphisms in Alzheimer disease
dc.typeArticle

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