Inhibiting Mitochondrial Transcription to Model Alzheimer's Disease

Our findings indicate IMT1 treatment successfully reduces mitochondrial transcription as revealed by lower mt-RNA and protein levels. Additionally, SY5Y treatment resulted in lower mtDNA copy numbers, aligning with lower mtDNA levels found in AD patients. Further, the decline in SY5Y mitochondrial activity suggests IMT1 induces mitochondria dysfunction. These findings indicate our model initiates mitochondrial dysfunction while demonstrating AD like characteristics, enabling us to use IMT1 treatment to model and study AD. Additional studies are ongoing to further characterize DNA, RNA, protein, enzymatic, and metabolic changes in both cell lines.