Open Access. Powered by Scholars. Published by Universities.®
- Discipline
- Keyword
Articles 1 - 2 of 2
Full-Text Articles in Enzymes and Coenzymes
Investigating Tau Pathology In The Retina And Anterior Segment Structures Of The Eye In A 3-Nitropropionic Acid–Induced Tauopathy Mouse Model, Mohamed Sayed Ahmed Abdel-Kader Qasem
Investigating Tau Pathology In The Retina And Anterior Segment Structures Of The Eye In A 3-Nitropropionic Acid–Induced Tauopathy Mouse Model, Mohamed Sayed Ahmed Abdel-Kader Qasem
Theses and Dissertations
Background and Objectives: Alzheimer's disease, the most prevalent neurodegenerative disorder in older adults, is characterized by accumulation of hyperphosphorylated tau and amyloid-beta (Aβ) plaques in the central nervous system. Given the retina's shared embryological origin with the brain, its direct neural connectivity via the optic nerve, and similarities in vasculature and age-related degeneration patterns, retinal pathology may serve as an early, non-invasive biomarker for Alzheimer's disease. This study employed 3-nitropropionic acid (3NP) as a pathway-specific tauopathy model driven by mitochondrial dysfunction. The study particularly aimed to investigate whether retinal and corneal tau pathology reflects underlying tau-related neurodegeneration triggered by …
Impact Of Intracellular Glutathione Depletion On Neutral Sphingomyelinase In Human Hepatoma Hepg2 Cells, Marie Tanios
Impact Of Intracellular Glutathione Depletion On Neutral Sphingomyelinase In Human Hepatoma Hepg2 Cells, Marie Tanios
Theses and Dissertations
Introduction: Incidence of hepatocellular carcinoma (HCC) has been increasing dramaticallyandliver cancer is the fifth most common cancer globally. Increasing sphingomyelin (SM) hydrolysis via activation of the cell surface membrane-associated neutral sphingomyelinase (nSMase) has been linked to cell proliferation and apoptosis. Glutathione (GSH) depletion was reported to mediate induction of apoptosis via nSMase activation. On the other hand, other studies reported that GSH protected cancer cells against apoptosis. We hypothesized that GSH synthesis inhibition with buthioninesulfoximine (BSO) increases HepG2 cell proliferation. Objectives: The aim of the current study wasto investigate the effect of GSH depletion using BSO on HepG2 cell proliferation …