Researcher:
Akşahin, İzel Cemre

Profile Picture
ORCID

OrgUnit Logo
Organizational Unit

Job Title

PHD Student

First Name

İzel Cemre

Last Name

Akşahin

Name

Name Variants

Akşahin, İzel Cemre

Email Address

Birth Date

Filters

20243

Advanced Search

Filter by

Settings

Researcher Of Publications: search.filters.isAuthorOfPublication.62e9e1e4-4621-4ff6-b8c1-6f93b1253fac

Search Results

Now showing 1 - 3 of 3
  • Placeholder
    PublicationMetadata only
    Correction: oxidatively-induced DNA base damage and base excision repair abnormalities in siblings of individuals with bipolar disorder DNA damage and repair in bipolar disorder
    (Springer Nature, 2024) Çelik, Hidayet Ece Arat; Yilmaz, Selda; Aksahin, Izel Cemre; Kendirlioglu, Burcu Kok; Corekli, Esma; Dal Bekar, Nazli Ecem; Celik, Omer Faruk; Yorguner, Nese; Ozturk, Bilge Targitay; Islekel, Huray; Ozerdem, Aysegul; Tuna, Gam; Akşahin, İzel Cemre; Ceylan, Deniz; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Graduate School of Health Sciences; School of Medicine
    Correction to: Translational Psychiatryhttps://doi.org/10.1038/s41398-024-02901-3, published online 24 May 2024 In this article the funding from ‘[2021.KB.SAG.047]’ was omitted. The corrected acknowledgment should read: This research was funded by the Dokuz Eylul University Scientific Research Project Scholarship (2021.KB.SAG.047) and LithiumAssociation Scholarship. The original article has been corrected.
  • Placeholder
    PublicationMetadata only
    Oxidatively-induced DNA base damage and base excision repair abnormalities in siblings of individuals with bipolar disorder DNA damage and repair in bipolar disorder
    (SpringerNature, 2024) Celik, Hidayet Ece Arat; Yilmaz, Selda; Kendirlioglu, Burcu Kok; Corekli, Esma; Dal Bekar, Nazli Ecem; Celik, Omer Faruk; Yorguner, Nese; Oztuerk, Bilge Targitay; Islekel, Hueray; Ozerdem, Ayseguel; Akan, Pinar; Tuna, Gamze; N/A; Akşahin, İzel Cemre; Ceylan, Deniz; Koç University Research Center for Translational Medicine (KUTTAM); School of Medicine; Graduate School of Health Sciences; Koç University Hospital
    Previous evidence suggests elevated levels of oxidatively-induced DNA damage, particularly 8-hydroxy-2'-deoxyguanosine (8-OH-dG), and abnormalities in the repair of 8-OH-dG by the base excision repair (BER) in bipolar disorder (BD). However, the genetic disposition of these abnormalities remains unknown. In this study, we aimed to investigate the levels of oxidatively-induced DNA damage and BER mechanisms in individuals with BD and their siblings, as compared to healthy controls (HCs). 46 individuals with BD, 41 siblings of individuals with BD, and 51 HCs were included in the study. Liquid chromatography-tandem mass spectrometry was employed to evaluate the levels of 8-OH-dG in urine, which were then normalized based on urine creatinine levels. The real-time-polymerase chain reaction was used to measure the expression levels of 8-oxoguanine DNA glycosylase 1 (OGG1), apurinic/apyrimidinic endonuclease 1 (APE1), poly ADP-ribose polymerase 1 (PARP1), and DNA polymerase beta (POL beta). The levels of 8-OH-dG were found to be elevated in both individuals with BD and their siblings when compared to the HCs. The OGG1 and APE1 expressions were downregulated, while POL beta expressions were upregulated in both the patient and sibling groups compared to the HCs. Age, smoking status, and the number of depressive episodes had an impact on APE1 expression levels in the patient group while body mass index, smoking status, and past psychiatric history had an impact on 8-OH-dG levels in siblings. Both individuals with BD and unaffected siblings presented similar abnormalities regarding oxidatively-induced DNA damage and BER, suggesting a link between abnormalities in DNA damage/BER mechanisms and familial susceptibility to BD. Our findings suggest that targeting the oxidatively-induced DNA damage and BER pathway could offer promising therapeutic strategies for reducing the risk of age-related diseases and comorbidities in individuals with a genetic predisposition to BD.
  • Placeholder
    PublicationMetadata only
    Integrating mitoepigenetics into research in mood disorders: a state-of-the-art review
    (Frontiers Media Sa, 2024) Arat-Çelik, Hidayet Ece; Ceylan, Deniz; Akşahin, İzel Cemre; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); School of Medicine; Graduate School of Health Sciences
    Mood disorders, including major depressive disorder and bipolar disorder, are highly prevalent and stand among the leading causes of disability. Despite the largely elusive nature of the molecular mechanisms underpinning these disorders, two pivotal contributors-mitochondrial dysfunctions and epigenetic alterations-have emerged as significant players in their pathogenesis. This state-of-the-art review aims to present existing data on epigenetic alterations in the mitochondrial genome in mood disorders, laying the groundwork for future research into their pathogenesis. Associations between abnormalities in mitochondrial function and mood disorders have been observed, with evidence pointing to notable changes in mitochondrial DNA (mtDNA). These changes encompass variations in copy number and oxidative damage. However, information on additional epigenetic alterations in the mitochondrial genome remains limited. Recent studies have delved into alterations in mtDNA and regulations in the mitochondrial genome, giving rise to the burgeoning field of mitochondrial epigenetics. Mitochondrial epigenetics encompasses three main categories of modifications: mtDNA methylation/hydroxymethylation, modifications of mitochondrial nucleoids, and mitochondrial RNA alterations. The epigenetic modulation of mitochondrial nucleoids, lacking histones, may impact mtDNA function. Additionally, mitochondrial RNAs, including non-coding RNAs, present a complex landscape influencing interactions between the mitochondria and the nucleus. The exploration of mitochondrial epigenetics offers valuable perspectives on how these alterations impact neurodegenerative diseases, presenting an intriguing avenue for research on mood disorders. Investigations into post-translational modifications and the role of mitochondrial non-coding RNAs hold promise to unravel the dynamics of mitoepigenetics in mood disorders, providing crucial insights for future therapeutic interventions.