First author Gianna Fote was recently interviewed by the Journal of Cell Science for a newly-published paper. She provided commentary on her team’s new findings for UCI MIND:
“In our recently published work we studied intracellular trafficking of Apolipoprotein E (APOE), a lipid-carrying protein. The APOE4 isoform of this protein is the biggest genetic risk factor for late-onset Alzheimer’s disease. We found that that APOE can be degraded by a process called autophagy, a process in which cellular waste is transported to an acidic organelle called the lysosome. The APOE4 isoform accumulates in the lysosome and causes increased induction of autophagy but ultimately impaired lysosomal clearance. Multiple types of autophagy appear to contribute to APOE degradation, including macroautophagy and chaperone-mediated autophagy. Understanding the pathways responsible for degradation of APOE and how the APOE4 isoform may affect those pathways may offer insights into the types of disease-modifying therapies that could one day benefit patients suffering from AD.”
Read about her work in Autophagy Reports >
