Cells use autophagy to export toxic proteins in Alzheimer’s disease

What is it about?

Cells normally rely on a protein called ubiquitin to mark damaged proteins for disposal. In Alzheimer’s disease, an abnormal form of ubiquitin, known as UBB+1, is produced due to errors during gene expression and can build up inside cells. This buildup is toxic and places cells under stress. Most studies have focused on how cells try to destroy such harmful proteins, but what happens when degradation is not enough has been unclear. In this study, we show that cells can use an alternative protective strategy: instead of only breaking down UBB+1, they actively package and export it out of the cell using a specialized recycling pathway called autophagy. This process depends on a helper protein called p62, which recognizes UBB+1 and directs it for secretion. Our findings reveal an unexpected way cells defend themselves against toxic protein accumulation, expanding how we think about protein quality control in neurodegenerative disease.

Featured Image

Photo by Rad Cyrus on Unsplash

Photo by Rad Cyrus on Unsplash

Why is it important?

Most studies focus on how cells destroy toxic proteins. Our work is unique because it shows that cells can actively export a harmful Alzheimer’s-linked protein when degradation fails. This offers a new way of thinking about how cells protect themselves under stress.

Perspectives