Akademik Veri Yönetim Sistemi
Molecular Biology Reports, cilt.53, sa.1, 2026 (SCI-Expanded, Scopus)
Background: Tau pathology is increasingly recognized as a driver of metabolic dysfunction in neurodegenerative diseases, extending beyond protein aggregation to include impairments in glucose metabolism and redox homeostasis. However, how metabolic cofactors affect tau-associated metabolic stress remains incompletely understood. Methods and Results: In this study, we employed a fission yeast (Schizosaccharomyces pombe) model expressing human tau to investigate the effects of vitamin B6 on glucose metabolism and cellular redox balance under glucose-limited conditions in tau-expressing cells. Cells were treated with vitamin B6 and analyzed for tau expression and phosphorylation, glucose consumption, NAD⁺/NADH ratio, and the expression of selected glucose metabolism–related genes under glucose starvation conditions. Vitamin B6 treatment was associated with a reduction in tau protein expression and phosphorylation at specific residues (S262, S396, S404). In addition, vitamin B6 affected glucose metabolism–related gene expression and was accompanied by modest changes in glucose consumption and redox balance. These effects were observed in both control and tau-expressing cells, although the patterns of response differed between the two conditions. While vitamin B6 generally enhanced the expression of glucose utilization–related genes in control cells, its effects in tau-expressing cells were more variable, indicating altered metabolic regulation under tau-associated stress. Conclusions: These findings suggest that vitamin B6 may contribute to cellular metabolic adaptation under tau-induced stress. This study demonstrates the usefulness of fission yeast as a tractable model for examining metabolic aspects of tau pathology and provides insight into how metabolic cofactors influence tau-associated cellular stress.