Seçil AKYILDIZ DEMİR

Mühendislik Fakültesi, Biyomühendislik Bölümü, Biyomühendislik Bölümü

Research areas: Natural Sciences, Health Sciences, Engineering and Technology, Neurobiology, Bioinformatics, Biotechnology, Molecular Biology and Genetics, Life Sciences

Publications

• Computational Investigation of Flavonoid￾Associated Molecular Pathways in Astrogliosis Modulation (2026)
• Comprehensive microRNA-seq transcriptomic analysis of Tay-Sachs disease mouse neuroglia revealed distinct miRNA profiles (2025)
• In-depth miRNA profiling uncovers unique microRNA signatures in the neuroglia of the Tay-Sachs disease mouse model (2025)
• Miglustat treatment reverses altered secondary lipids and inflammatory markers in lysosomal sialidase Neu1 deficient fibroblasts (2025)
• Intracerebroventricular delivery of ASO in combination with anti-inflammatory and ketogenic diet treatment reversed neuropathology in the Tay-Sachs disease mouse model (2025)
• A Comprehensive microRNA-seq Transcriptomic Analysis of Tay-Sachs Disease Mice Revealed Distinct miRNA Profiles in Neuroglial Cells (2025)
• Abnormally accumulated GM2 ganglioside contributes to skeletal deformity in Tay-Sachs mice (2024)
• Silencing of B4Galnt1 Gene Prevents GM2 Accumulation in Tay-Sachs Cells (2024)
• Induction of Exocytosis Rescues Lysosomal GM2 Accumulation in Tay-Sachs Disease (2024)
• In silico molecular docking of natural anti neuroinflammatory flavonoids on reactive astrogliosis (2023)
• Analysis of Brain Lipids in the Early-Onset Tay-Sachs Disease Mouse Model With the Combined Deficiency of β-Hexosaminidase A and Neuraminidase 3 (2022)
• Sialidase neu4 deficiency is associated with neuroinflammation in mice (2021)
• Brain lipid profile of early onset Tay-Sachs disease mouse model (2020)
• Alteration in redox homeostasis in early-onset Tay-Sachs disease mouse model (2020)
• GM2 ganglioside accumulation causes neuroinflammation and behavioral alterations in a mouse model of early onset Tay-Sachs disease (2020)
• Identification of cytoplasmic sialidase NEU2-associated proteins by LC-MS/MS (2019)
• Abnormal GM2 accumulation alters the function of the autophagic pathway in early-onset Tay-Sachs disease mouse model (2018)
• Anormal GM2 Birikiminin Erken Başlangıçlı Tay-Sachs Hastalığı Fare Modelinde Nöroinflamatik ve DavranışsalEtkisi (2018)
• Sapozin A Eksikliği ve Bozulmuş Otofaji (2018)
• Anormal GM2 Birikiminin Erken Başlangıçlı Tay-Sachs Fare Modellerindeki Otofajik Akışa Etkisi (2018)
• Murine Sialidase Neu3 facilitates GM2 degradation and bypass in mouse model of Tay-Sachs disease (2018)
• The Second Case of Saposin A Deficiency and Altered Autophagy (2018)
• The Second Case of Saposin A Deficiency and Altered Autophagy (2018)
• Effects of cell-mediated osteoprotegerin gene transfer and mesenchymal stem cell applications on orthodontically induced root resorption of rat teeth (2017)
• Behavioral analysis of mouse model with combined deficiencies of β-Hexosaminidase A and sialidase Neu3 reveals motor coordination impairment and memory loss (2016)
• Lysosomal Cathepsin A Plays a Significant Role in the Processing of Endogenous Bioactive Peptides (2016)
• Neuraminidase-1 contributes significantly to the degradation of neuronal B-series gangliosides but not to the bypass of the catabolic block in Tay-Sachs mouse models (2015)
• Altered vasoactive peptide composition in the tissues of Cathepsin A deficient mice (2014)
• Mice with combined deficiencies of β-Hexosaminidase A and Sialidase Neu3 mimic the fundamental aspects of the neurological abnormalities of Tay-Sachs disease due to accumulation of ganglioside: New hope for Tay-Sachs patients and families (2014)
• Lysosomal Cathepsın A Defıcıent Mouse Model Shows Altered Vasoactıve Peptıd Endothelın-I (Et-I) Level in Serum and Organs (2013)
• Immunohistochemical study of lysosomal Cathepsin A deficient mouse model shows accumulation of vasoactive peptides in brain. (2013)

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