PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7645

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Author: search.filters.author.Nazli, D.

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  • Article
    Epigallocatechin Gallate and Punicalagin Combination Reduces Aβ Aggregation and Promotes Neurogenesis in Adult Zebrafish Brain
    (John Wiley and Sons Inc, 2026) Nazli, D.; Ipekgil, D.; Poyraz, Y.K.; Can, K.; Okmen, I.; Turhanlar-Sahin, E.; Ozhan, G.
    Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and behavioral alterations. The pathogenesis of AD involves the accumulation of amyloid-beta (Aβ) plaques and the hyperphosphorylated tau proteins, which disrupt neuronal function and trigger neuroinflammation. This study explores the therapeutic potential of epigallocatechin gallate (EGCG) and punicalagin (PU) in mitigating Aβ-induced toxicity using an adult zebrafish model of AD. Our results demonstrate that the EGCG + PU combination significantly reduces Aβ accumulation, protects against cellular damage, suppresses acetylcholinesterase (AChE) activity, and normalizes the expression of amyloidogenic and AD-related genes. Additionally, EGCG + PU treatment alleviates neuroinflammation by suppressing glial activation, including reductions in L-plastin and proinflammatory cytokine expression, while promoting neuronal recovery through mechanisms of neurogenesis and neuroprotection. Notably, the combination treatment restored neuronal density and improved behavioral outcomes by alleviating anxiety- and aggression-like behaviors associated with Aβ toxicity. These results underscore the synergistic neuroprotective effects of EGCG + PU, highlighting their potential as a novel therapeutic approach for mitigating the pathological, behavioral, and inflammatory aspects of AD. © 2026 Wiley Periodicals LLC.
  • Review
    Citation - Scopus: 2
    Wnt/β-catenin Signaling in Central Nervous System Regeneration
    (2025) Nazli, D.; Bora, U.; Ozhan, G.
    The Wnt/β-catenin signaling pathway plays a pivotal role in the development, maintenance, and repair of the central nervous system (CNS). This chapter explores the diverse functions of Wnt/β-catenin signaling, from its critical involvement in embryonic CNS development to its reparative and plasticity-inducing roles in response to CNS injury. We discuss how Wnt/β-catenin signaling influences various CNS cell types-astrocytes, microglia, neurons, and oligodendrocytes-each contributing to repair and plasticity after injury. The chapter also addresses the pathway's involvement in CNS disorders such as Alzheimer's and Parkinson's diseases, psychiatric disorders, and traumatic brain injury (TBI), highlighting potential Wnt-based therapeutic approaches. Lastly, zebrafish are presented as a promising model organism for studying CNS regeneration and neurodegenerative diseases, offering insights into future research and therapeutic development. © 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.
  • Article
    Citation - WoS: 3
    Citation - Scopus: 3
    Evaluation of the Effects of Carbamazepine-Loaded Chitosan-Coated Plga-Zein Nanoparticles on Pilocarpine-Induced Seizure Model in Zebrafish Larvae: Developmental Toxicity and Behavioral Assays
    (Oxford University Press, 2025) Alak, G.; Yıldırım, S.; Ugur Kaplan, A.B.; Köktürk, M.; Nazli, D.; Gözegir, B.; Cetin, M.
    Epilepsy, the most common neurological disorder worldwide, is characterized by sudden paroxysmal brain activity, which can be generalized or focal. Extensive research has explored various treatment strategies for this condition. Our study used a pilocarpine (PL)-induced seizure model in zebrafish (Danio rerio) embryos and larvae to assess the effects of carbamazepine (CBZ)-loaded chitosan-coated PLGA-Zein nanoparticles (NPs) over 96 hr. We evaluated the developmental toxicity (mortality, malformation, and larval hatching), behavioral changes (sensorimotor reflexes), and histopathological and immunohistochemical alterations in brain tissue, focusing on 5-hydroxytryptamine receptor 4 (5HT4), and brain and muscle ARNT-like 1 (BMAL1) expressions. Our findings revealed high mortality and malformation rates in groups treated with pure CBZ (PL + CBZ 50 and PL + CBZ 100). These groups also exhibited delayed hatching and impaired sensorimotor reflexes. In contrast, the CBZ-NP-treated groups (PL + CBZ NP 50 and PL + CBZ NP 100) showed hatching rates comparable with the control group, with significantly lower mortality and malformation rates compared with pure CBZ-treated groups. Moreover, intense cytoplasmic expression of 5HT4 and BMAL1 was observed in neuropils of the PL + CBZ 100 group. This study highlights the potential of CBZ-loaded NPs in reducing developmental toxicity and adverse neurological effects associated with pure CBZ treatment in seizure models. © The Author(s) 2025. Published by Oxford University Press on behalf of the Society of Environmental Toxicology and Chemistry. All rights reserved.