Our Foundation is the implementation partner of the Aligning Science Across Parkinson’s (ASAP) initiative, which is fostering collaboration and resources to better understand the underlying causes of Parkinson’s disease.
ASAP is a coordinated research initiative to advance targeted basic research for Parkinson’s disease. This initiative, announced in 2019, builds on the significant strides made by the research community, funders, other experts and strategists around the world.
With input across sectors and disciplines, ASAP has developed a strategic roadmap to collectively tackle field-wide challenges:
- Support meaningful, multidisciplinary collaboration
- Generate research-enabling resources
- Democratize data
Led by Nobel Laureate Dr. Randy Schekman and Dr. Ekemini Riley, ASAP is working with The Michael J. Fox Foundation to implement its programs. ASAP was incubated at the Milken Institute Center for Strategic Philanthropy with support from the Sergey Brin Family Foundation.
Visit www.parkinsonsroadmap.org to read more on the history and vision of the ASAP initiative.
Randy Schekman, PhD
Scientific Director, ASAP
Ekemini A. U. Riley, PhD
Managing Director, ASAP
The ASAP initiative’s investment in basic research is positioning the field for a seismic shift in understanding of Parkinson’s onset and progression. MJFF is designing our research strategy to complement ASAP programs with continued funding across the development pipeline, from basic discovery work through clinical trials and post-market analysis.
For our latest RFAs, visit our Funding Opportunities page.
ASAP Implementation Partner
In parallel, we are working with ASAP as its implementation partner and have been involved since the initiative’s inception.
The scientific community’s recognition and trust of The Michael J. Fox Foundation as a research partner is an invaluable asset in scaffolding these programs and building toward our shared goals.
– Randy Schekman, PhD, ASAP Scientific Director
ASAP has leveraged our grantmaking infrastructure to accept and review proposals and to issue grants to its Collaborative Research Network and its Global Parkinson’s Genetics Program (GP2). In addition, MJFF staff provides business operations support such as coordinating and managing resource acquisitions and data sharing.
Through our partnership, ASAP has also signed on to other consortia that count MJFF as a partner. ASAP is now a member of the Accelerating Medicines Partnership Parkinson’s disease (AMP PD) program managed by FNIH (the Foundation for the NIH) and uniting government, industry and non-profits to support biomarker and target discovery work. (MJFF is a founding member.)
And ASAP is partnering in our landmark study, the Parkinson’s Progression Markers Initiative (PPMI). ASAP support is allowing PPMI to significantly expand its enrollment — bringing together a larger and more diverse group of individuals to increase understanding around how Parkinson's develops and changes over time.
A tenet of the ASAP strategy is research-enabling resources, and the initiative is supporting large-scale programs to build and share a variety of tools.
Global Parkinson’s Genetics Program (GP2)
GP2 is an ambitious five-year program to genotype >150,000 volunteers around the world to further understand the genetic architecture of Parkinson’s disease. Underlying data, analytical processes, and results from GP2 will be made available to the research community as quickly as possible, with minimal barriers to access and use.
Parkinson’s Progression Markers Initiative (PPMI)
ASAP has devoted significant support to our longitudinal PPMI study and has joined the PPMI steering committee to direct the future of this valued resource. PPMI aims to enroll more than 4,000 participants across a variety of cohorts including many with Parkinson’s risk factors who may help learn about how to predict, detect and stop the disease at its earliest stages. All PPMI data is de-identified and open to the researcher community (in addition to available biosamples).
ASAP is funding multidisciplinary research teams to form the ASAP Collaborative Research Network, which will address key knowledge gaps in the basic mechanisms that contribute to Parkinson’s development and progression.
Circuitry and Brain-Body Interactions RFA
Biology of PD-associated Genes and Neuro-Immune RFAs
Through its first funding program, ASAP is supporting 21 teams investigating either biology of Parkinson’s-related genes and/or neuro-immune interactions. All data resulting from this funded work will be made available to the scientific community at large at the earliest opportunity.
The funded teams and projects are:
Mapping the LRRK2 Signaling Pathway and Its Interplay with Other Parkinson’s Disease Components
Dario Alessi, Monther Abu-Remaileh, Miratul Muqit, Suzanne Pfeffer
This project seeks to understand the molecular and cellular consequences of Rab GTPase phosphorylation by pathogenic LRRK2 kinase and its effects on the downstream biology of primary cilia, lysosomes, and mitochondria.
From Cancer Associations to Altered Immunity in the Pathogenesis of Parkinson’s Disease
Xiqun Chen, Timothy Chan, Weiyi Peng, Michael Schwarzschild
This study investigates altered immunity in dopaminergic neurodegeneration in the context of genetic alterations linking Parkinson’s disease and cancer.
Impaired Integration of Organelle Function in Parkinson’s Disease
Pietro De Camilli, Shawn Ferguson, Kallol Gupta, Karin Reinisch, Timothy Ryan, PhD
This project, which is focused on selected PD genes, hopes to uncover the role of endolysosomal dysfunction and of impaired cross-talk between the endolysosomal system and mitochondria in PD pathogenesis.
Role of PD-related Proteins as Drivers of Disease through Modulation of Innate and Adaptive Immunity
Michel Desjardins, Samantha Gruenheid, Heidi McBride, Jo Anne Stratton, Louis-Eric Trudeau
This research team will investigate the contribution of autoimmune mechanisms in the pathophysiological process leading to Parkinson’s disease at the cell level, as well as in mouse models and human samples.
Tracing the Origin and Progression of Parkinson’s Disease through the Neuro-Immune Interactome
David Hafler, Sreeganga Chandra, Rui Chang, Noah Palm, Ramnik Xavier
This team will integrate cutting-edge technologies in neuroimmunology, single cell genomics, gut microbiome, and computational biology to determine at unprecedented depth whether Parkinson’s disease has the signature of autoimmune processes.
Dissecting the Mechanisms Underlying Disease Progression
John Hardy, Zane Jaunmuktane, Frances Platt, Mina Ryten, Maria Spillantini
This project will dissect the genetic and gene expression variability underlying differences in the rate of decline of PD and model this decline in cell and mouse models of disease.
Mechanisms Overwhelming Protein and Organelle Quality Control in Parkinson's Disease
J. Wade Harper, Ruben Fernandez-Busnadiego, Judith Frydman, Franz-Ulrich Hartl, Brenda Schulman,
This project will employ biochemical, cell biological and structural approaches to elucidate mechanisms overwhelming protein and organelle quality control in Parkinson’s with the goal of identifying potentially actionable therapeutic targets.
Mechanisms of Mitochondrial Damage Control by PINK1 and Parkin
James Hurley, Erika Holzbaur, Michael Lazarou, Sascha Martens, Eunyong Park
PINK1 and Parkin trigger the removal of damaged mitochondria, which are toxic to neurons. This project will use the most advanced mechanistic cell biology methods to determine how they do this.
Activation of Transposable Elements as a Trigger of Neuroinflammation in Parkinson’s Disease
Johan Jakobsson, Roger Barker, Molly Hammell, Agnete Kirkeby
This project will investigate if activation of transposable elements, which are viral-like sequences that make up half of our genome, causes inflammation in the brains of people with Parkinson’s disease.
In Vivo Approach to Elucidate the Pathobiology of Parkinson’s-associated Genes Using Human Diseased Neurons
Deniz Kirik, Jennifer Johnston, Clare Parish, Lachlan Thompson, Carolyn Sue
This project will use patient-derived cells from genetic forms of PD, studied in the environment of the living brain, as a unique paradigm to reveal cellular components of PD pathobiology.
Co-Pathologies Drive Neuroinflammation and Progression in PD
Jeffrey Kordower, Ashley Harms, Warren Hirst
This program will study the influence of co-pathologies that occur in PD, such as tau and beta amyloid, on inflammation and disease progression in murine and non-human primate models of PD.
Senescence in Parkinson’s Disease and Related Disorders
Michael Lee, Jose Bras, Darren Moore, Laura Niedernhofer
This project will determine if cellular senescence is a pathogenic component of Parkinson’s disease and test if drugs targeting senescent cells can be used as a disease-modifying therapy for PD.
Cellular Mechanism of LRRK2 in Health and Disease
Samara Reck-Peterson, Stefan Knapp, Andres Leschziner, Florian Stengel, Elizabeth Villa
This project will map the structural states of LRRK2, the most commonly mutated gene in familial Parkinson’s disease, on to its cellular interaction landscape to understand its function in health and disease.
Dissecting Genetic Interactions of Parkinson’s Disease-associated Risk Loci
Donald Rio, Helen Bateup, Luke Gilbert, Dirk Hockemeyer, Frank Soldner
This project uses state-of-the-art functional genomics approaches to identify gene expression and RNA splicing signatures in human stem cell-derived neurons and mice carrying familial and GWAS-nominated Parkinson’s risk genes.
Genome-Microbiome Axis in the Cause of Parkinson Disease: Mechanistic Insights and Therapeutic Implications from Experimental Models and a Genetically Stratified Patient Population
Anthony Schapira, Fabio Blandini, Michela Deleidi, Donato Di Monte, Stanislav Ehrlich
This team will investigate the importance and effect of intestinal bacteria on Parkinson’s disease development in people with glucocerebrosidase mutations. The project will involve human participants and cell and animal models.
Parkinson5D: Deconstructing Proximal Disease Mechanisms across Cells, Space, and Progression
Clemens Scherzer, Xianjun Dong, Mel Feany, Joshua Levin, Su-Chun Zhang
Parkinson5D will hunt for the proximal mechanisms of Parkinson’s disease using five-dimensional brain cell sequencing and genetically engineered avatars in fruit flies and stem cells.
Defining the Cellular and Molecular Determinants of Variable Genetic Penetrance in Parkinson’s Disease
Lorenz Studer, Gist Croft, Vikram Khurana, Jian Peng, Joseph Powell
This project uses advanced human patient stem cell models to understand how the interplay between genetics, glia-neuronal interactions and aging shape an individual’s risk of developing Parkinson’s disease.
Adaptive Immunity in the Etiology and Progression of Parkinson’s Disease
David Sulzer, Cecilia Arlehamn, Ashley Harms, Sarkis Mazmanian
This team investigates the adaptive immune system and autoimmunity in Parkinson’s disease, particularly roles for antigen presentation and T cells in the periphery and the enteric and central nervous systems.
IMPACT-PD - Implications of Polyamine and Glucosylceramide Transport in Parkinson’s Disease
Peter Vangheluwe, Tim Ahfeldt, Veerle Baekelandt, Joseph Lyons, Ellen Sidransky
IMPACT-PD focuses on the new biology of lysosomal polyamine and glucosylceramide transporters that are genetically implicated in Parkinson’s disease, and how they intersect with disease pathways converging at the lysosome.
Understanding Inherited and Acquired Genetic Variation in Parkinson’s Disease through Single-Cell Multi-omics Analyses
Thierry Voet, Stein Aerts, Guy Boeckxstaens, Christos Proukakis, Bernard Thienpont
This project will provide a multiomics atlas of >4,500,000 million single cells from brain and gut to identify Parkinson’s disease-relevant genes and cell (sub)types, and their perturbation by genetic variation.
Mapping the PD Brain: Oligomer-driven Functional Genomics
Nicholas Wood, Sonia Gandhi, Steven Lee, Mina Ryten, Michele Vendruscolo
This study will use single molecule techniques to identify the oligomers of alpha-synuclein in the Parkinson’s brain and harness single cell transcriptomics and genomics to delineate molecular pathways to disease.