Abstract 1509 Lysosomal TMEM106b prevents Tau misregulation caused by mitochondrial dysfunction through complex 1 inhibition

Mitochondrial dysfunction is a hallmark of numerous neurodegenerative diseases, often resulting in the misregulation of critical cellular proteins, such as Tau. Inhibition of mitochondrial complex 1 (NADH oxidoreductase) disrupts cellular energy metabolism and is linked to Tau pathology. Under these conditions, lysosomal TMEM106b has emerged as a key regulator of cellular homeostasis. Despite the known role of mitochondrial complex 1 inhibition in neurodegenerative diseases, the interplay between mitochondria and lysosomes in this context remains unclear.