ASAP is committed to accelerating the pace of discovery and informing a path to a cure for Parkinson’s disease through collaboration, research-enabling resources, and data sharing. We’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.


Rodent models based on endolysosomal genes involved in Parkinson’s disease

This review summarizes parkinsonian phenotypes in rodent models targeting genes that have a role in endolysosomal pathways and future steps to better understand the contribution of endolysosomal dysfunction to PD.


Lysosomal dysfunction in neurodegeneration: emerging concepts and methods

This review summarizes key technological advances that have led to a better understanding of the contribution of the lysosome to neurodegeneration and highlights key questions to be addressed moving forward.


The lysosome as a master regulator of iron metabolism

This review focuses on the role that the lysosome plays in maintaining iron homeostasis and how lysosomal iron dysregulation contributes to disease.


Western blot protocol for detecting ATP10B in mouse/rat brain

This protocol describes the procedure for detection of ATP10B in rat and mouse brain tissue by Western blotting


ATP13A2-mediated endo-lysosomal polyamine export counters mitochondrial oxidative stress

Loss-of-function of ATP13A2, an endo-lysosomal transporter that pumps polyamines into the cytosol, is associated with PD. ATP13A2 dysfunction causes polyamine accumulation within the lysosome and lysosomal rupture. The authors found a conserved cellular protective pathway involving ATP13A2-mediated lysosomal spermine export to provide protection against mitochondrial toxins.


ATP13A2 Regulates Cellular α-Synuclein Multimerization, Membrane Association, and Externalization

ATP13A2 loss-of-function mutations cause lysosomal deficiency and are linked to Parkinson’s disease and alpha-synuclein pathology. The authors found that loss of ATP13A2 disrupts lysosomal membrane integrity and causes alpha-synuclein multimerization. Further, they showed that increased levels of ATP13A2 had a protective effect on alpha-synuclein aggregation.