PRKN and Alzheimer disease: We have also examined the capacity of altered heparan sulfate biosynthesis to provide protection from cell loss in a Presenilin model of Alzheimer’s Disease (AD), or deficits in mitochondrial surveillance mediated by mutations in parkin, the homolog of PARK2. In both of these models of human neurodegenerative disorders, altering heparan sulfate biosynthesis rescued cell loss, showing that changes in heparan sulfate can affect the capacity of cells to tolerate a variety of cellular stresses.