Nazlı, Dilek

Profile URL
https://hdl.handle.net/11147/16597
Name Variants
Nazlı, Makbule Dilek
Job Title
Email Address
makbulenazli@iyte.edu.tr
Main Affiliation
04.03. Department of Molecular Biology and Genetics
Status
Current Staff
Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID
HLX-8000-2023

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
Research Products
ZERO HUNGER2
ZERO HUNGER
0
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
2
Research Products
QUALITY EDUCATION4
QUALITY EDUCATION
0
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GENDER EQUALITY5
GENDER EQUALITY
0
Research Products
CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
0
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
0
Research Products
DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
Research Products
INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
0
Research Products
REDUCED INEQUALITIES10
REDUCED INEQUALITIES
0
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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CLIMATE ACTION13
CLIMATE ACTION
0
Research Products
LIFE BELOW WATER14
LIFE BELOW WATER
0
Research Products
LIFE ON LAND15
LIFE ON LAND
0
Research Products
PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
0
Research Products
PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
0
Research Products
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Scholarly Output

2

Articles

1

Views / Downloads

810/664

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

7

Scopus Citation Count

8

Patents

0

Projects

0

WoS Citations per Publication

3.50

Scopus Citations per Publication

4.00

Open Access Source

2

Supervised Theses

0

JournalCount
48th FEBS Congress1
Molecular Neurobiology1
Current Page: 1 / 1

Scopus Quartile Distribution

Competency Cloud

GCRIS Competency Cloud
Author of Publication: search.filters.isAuthorOfPublication.098234ca-2a9a-462e-947c-16c0e9e38226

Scholarly Output Search Results

Now showing 1 - 2 of 2
  • Conference Object
    Investigation of the role of Wnt/β-catenin signaling in development of Alzheimer's disease in a zebrafish model of mmyloid-β toxicity
    (Wiley, 2024) Nazlı, Dilek; Nazlı, Dilek; Ipekgil, D.; Özhan, Güneş; Poyraz, Y. K.; Catak, B.; Sahin, E. Turhanlar; Özhan, Güneş; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    The Wnt/β-catenin signaling pathway, an evolutionarily conserved and pivotal pathway associated with synapse formation in adulthood, plays a crucial role in Alzheimer's disease (AD). AD, marked by various pathologies, is primarily linked to the accumulation of extracellular beta-amyloid plaques. The interplay between this accumulation and disruptions in the Wnt/β-catenin signaling pathway triggers synaptic degeneration, resulting in synaptic dysfunction and AD progression. In this study, we modeled AD induced by the Aβ42 peptide using adult transgenic (6XTCF) zebrafish. To establish the zebrafish AD model, we employed cerebroventricular microinjection (CVMI) with the Aβ42 peptide. Fish, anesthetized prior to CVMI, were positioned on a stable platform, and the Aβ42 peptide was injected into the telencephalon region of the brain by a capillary needle. Brain samples were collected on 1, 3, 4, 7, and 14 days post-CVMI (dpi) to analyze changes in Aβ42 peptide accumulation, the immune system response, synaptic degeneration, apoptosis, and the expression of genes related to proliferation using qPCR and immunofluorescent staining. To examine the role of the Wnt/β-catenin signaling pathway in the molecular mechanism of AD development, fish exhibiting high levels of regeneration on days 7 and 14 were treated with the IWR-1 drug, which inhibits the Wnt/β-catenin signaling by stabilizing the Axin2 protein, thereby suppressing the regenerative response. Our results revealed that the AD model manifested on 3dpi, with the regenerative response reaching its peak on 7dpi and 14dpi. Treatment with IWR-1 resulted in increased Aβ42 accumulation, accelerated synaptic degeneration, and elevated cell deaths in fish where the Wnt signaling pathway was inhibited. In conclusion, our adult zebrafish AD model is poised to elucidate the molecular mechanisms connecting the Wnt signaling pathway and AD, thereby contributing to the development of alternative therapeutic approaches for AD patients.
  • Article
    Citation - WoS: 7
    Citation - Scopus: 8
    High-Fat Diet Feeding Triggers a Regenerative Response in the Adult Zebrafish Brain
    (Springer, 2023) Azbazdar, Yağmur; Nazlı, Dilek; Özhan, Güneş; Nazlı, Dilek; İpekgil, Doğaç; Cucun, GÖkhan; Özhan, Güneş; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    Non-alcoholic fatty liver disease (NAFLD) includes a range of liver conditions ranging from excess fat accumulation to liver failure. NAFLD is strongly associated with high-fat diet (HFD) consumption that constitutes a metabolic risk factor. While HFD has been elucidated concerning its several systemic effects, there is little information about its influence on the brain at the molecular level. Here, by using a high-fat diet (HFD)-feeding of adult zebrafish, we first reveal that excess fat uptake results in weight gain and fatty liver. Prolonged exposure to HFD induces a significant increase in the expression of pro-inflammation, apoptosis, and proliferation markers in the liver and brain tissues. Immunofluorescence analyses of the brain tissues disclose stimulation of apoptosis and widespread activation of glial cell response. Moreover, glial activation is accompanied by an initial decrease in the number of neurons and their subsequent replacement in the olfactory bulb and the telencephalon. Long-term consumption of HFD causes activation of Wnt/β-catenin signaling in the brain tissues. Finally, fish fed an HFD induces anxiety, and aggressiveness and increases locomotor activity. Thus, HFD feeding leads to a non-traumatic brain injury and stimulates a regenerative response. The activation mechanisms of a regeneration response in the brain can be exploited to fight obesity and recover from non-traumatic injuries.