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.

Blog Post

A Blueprint for Training and Development in GP2

This blog written by Dr. Alastair Noyce and Dr. Sara Bandres-Ciga discusses GP2’s plan to train students and investigators and the new considerations as a result of the COVID-19 pandemic.

Blog Post

A letter to the patient community from Randy Schekman, ASAP Scientific Director

This blog written by Dr. Randy Schekman and Benjamin Stecher describes the motivation and beginnings of the ASAP initiative. It also includes a letter written to the PD comunity by Dr. Schekman.


A possible role for VPS13-family proteins in bulk lipid transfer, membrane expansion, and organelle biogenesis.

This review focuses on the structure and function of the VPS13 family of proteins and discusses the prevailing hypthoses in the field regarding its role in lipid transport.


ALS- and FTD-associated missense mutations in TBK1 differentially disrupt mitophagy

TBK1 mutations are linked to neurodegenerative disorders. The authors explored how TBK1 functions in PINK1/Parkin-dependent mitophagy and how mutations lead to disease. They found that TBK1 recruitment and kinase activity contributed to the clearance of damaged mitochondria (mitophagy). Further, they showed that TBK1 presence alone could disrupt the mitochondrial network. View preprint.

Blog Post

Applying for GP2 Data Access on the AMP® PD Platform

This blog written by Justin C. Solle, Claire Wegel, and Dr. Eline Appelmans outlines how to access GP2 on the AMP PD platform.


Assessing enrichment of proteins in the mitochondrial fraction in HEK cells

This is a method for measuring protein enrichment on mitochondria in various conditions. In the resulting Western blot, one can assess the level of contamination of other organelles in the enrichment prep.


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.


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.

Blog Post

Building Clinical and Genetic Data for GP2 in the Cohort Integration Working Group

This blog written by Dr. Huw Morris describes how the cohort integration working group within GP2 is working to harmonize clinical data.