Guide to Sharing De-Identified Human Subject Data
By onThe purpose of this document is to provide an overview of considerations for publishing de-identified, individual human subject data in preparation for publication. Human subject data may be classified as sensitive data, which are data that contain personal information, such as protected health information, and any other data that is likely to negatively harm an individual or community if publicly released. The ASAP Open Science Policy requires that sensitive data must be deposited to the extent allowed by the associated research ethics approval. If the data can be openly shared, then we require these data be deposited in a publicly accessible repository. If the data cannot be openly shared, but can be shared with restricted or controlled access, then it must be shared as restricted or controlled data, and come with instructions for how to request access to the data. Please note that we require that grantees collecting data from human participants to provide evidence that there has been satisfactory review and approval of the plan to collect and/or share such data from the appropriate ethics committee(s) (or evidence that no such approval is required).
Formatting Tabular Data Guide
By onThe purpose of this document is to provide guidance on how to properly format and share tabular data to increase accessibility and interoperability. The ASAP Open Science Policy requires that the data underlying all results reported in a manuscript be deposited in a publicly accessible repository. This must be done no later than time of publication and the dataset must be cited in the publication with a persistent identifier. To assist ASAP grantees in sharing usable tabular data and to ensure that they meet the ASAP data-sharing standards outlined in this document, the Open Science Team will review all ASAP-affiliated Zenodo dataset uploads.
Uploading Data to Zenodo Guide
By onThis document provides step-by-step instructions for how to upload datasets to Zenodo. The ASAP Open Science Policy requires all previously unpublished datasets that are included in a publication be deposited in a publicly accessible repository no later than time of publication and cited in the publication with their persistent identifier. We recommend Zenodo for tabular data and any data types that don't have a data type-specific repository.
Licensing Guide
By onThe purpose of this document is to provide background information on open access licenses and guidance on how to apply these licenses to preprints, publications, data, and software. The ASAP Open Science Policy requires that ASAP-funded preprints, publications, data, and code be licensed for reuse. For preprints, publications, and data, we require a CC BY 4.0 or CC0 license. For code, we recommend using the MIT License or another permissive license.
Investing in Open Science: Key Considerations for Funders
By onThe Aligning Science Across Parkinson’s (ASAP) initiative utilizes a comprehensive open science policy, which, in addition to requiring immediate free online access to all publications, also requires all newly-generated datasets, protocols, code, and key lab materials be shared by the time of publication. Moreover, preprints must be posted to a preprint repository by the time of manuscript submission to a journal for review. Here, we outline the potential costs associated with implementing and enforcing this open science policy. We recommend that funders take these considerations into account when investing in open science policies within the biomedical research ecosystem.
An ImageJ/FIJI Preprocessing Workflow for Multi-Series Confocal Microscopy Datasets Prior To CellProfiler Analysis
By onA workflow using ImageJ/FIJI aims to create three-slice MIPs from multi-series .czi files to capture weak signals. It involves extracting datasets, creating projections, and saving images for efficient analysis in CellProfiler.
Myeloid PINK1 represses mtDNA release and immune signaling that impacts neuronal pathology in patient-derived idiopathic PD models
By onPINK1 represses mtDNA release and STING/NF-κB activation in peripheral macrophages of PD model laying the foundation for understanding PINK1-related peripheral mechanisms in idiopathic PD and providing targets for further therapy development
A CellProfiler Pipeline for Quantification of p-SNCA in Mouse Striatal Cholinergic and Medium Spiny Neurons
By onBrain sections stained for pSNCA, DARPP-32, ChAT, and DAPI. Z-stacks processed into MIPs for analysis. Outputs include pSNCA intensity and neuronal mask area, normalised for cell type-specific burden using R script.
Dataset for Article “Presynaptic GABAA receptors control integration of nicotinic input onto dopaminergic axons in the striatum” by Brill-Weil et al
By onDopaminergic neuron axons have GABAARs and nAChRs that influence DA release. GABAAR antagonism enhances nAChR activity, while picrotoxin inhibits nAChRs, revealing GABAARs' role in regulating nicotinic input onto DA axons.
Primary Tabular Data for article “CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology” by Liao et al
By onMitochondrial dysfunction is linked to CHCHD2 mutation, causing altered protein interactions, glycolysis, and ROS, plus α-synuclein aggregation, and neurodegeneration. CHCHD2 accumulation leads to mitochondrial impairment and PD progression.
Processed Proteomics Data for Article “CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology” by Liao et al
By onMitochondrial dysfunction is linked to CHCHD2 mutation, causing disrupted protein interactions, metabolic shift to glycolysis, ROS elevation, and α-synuclein aggregation. CHCHD2 accumulation leads to neurodegeneration via impaired respiration.
Human Spatial Transcriptomics data for article “CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology” by Liao et al
By onMitochondrial dysfunction in Parkinson's disease involves CHCHD2 mutation leading to disrupted protein interactions, mitochondrial damage, glycolysis shift, increased ROS, and α-synuclein aggregation, linking to neurodegeneration.
2025: A Year in Review
We are proud to share how we impacted the Parkinson’s disease research field in 2025. Read our report to see how the infrastructure and processes we established are changing the way science is done and are generating significant momentum.
Bolen CosMx human Colon RNA and Protein code
By onRepository for the paper "Spatial single-cell multiomics..." includes CosMx assays, README files with scripts/data for analysis, and computational environment requirements. It also features a tissue microarray image showing morphology markers.
Multi-omics reveal critical differentiation target for Parkinson’s Disease-vulnerable midbrain dopaminergic neurons
By onWe describe a multiomic-guided strategy that enriches SOX6+ mDA neurons by combining enhancing Sonic Hedgehog agonism with prolonged Wnt activation. This work is a reproducible differentiation platform for generating the PD-susceptible mDA subtype
Tansey Stool Meso Scale Discovery
By onStool samples of healthy controls and individuals with either PD or IBD analyzed for chemokines, cytokines, and ferritin levels using U-PLEX and R-PLEX assays on Quickplex MSD instrument.
Bolen Human Sigmoid Colon Protein CosMx Datasets
By onProtein dataset from NanoString CosMx includes sigmoid colon samples from healthy controls, Parkinson's disease, and inflammatory bowel disease patients for analysis.
Tansey Plasma Meso Scale Discovery
By onPlasma samples from individuals with Parkinson's disease, inflammatory bowel disease, or healthy controls were analyzed to measure chemokines and cytokines. The study used Quickplex MSD instrument following manufacturer's protocol.
Bolen Human Sigmoid Colon RNA CosMx Dataset
By onNanoString CosMx RNA dataset from human sigmoid colon of healthy controls, Parkinson's Disease, or inflammatory bowel disease exported for analysis.
Striatal ensembles specify and control granular forelimb actions
By onThe striatum plays a crucial role in controlling movements and learning. These results reveal specific ensembles of both D1- and D2-MSNs causally control specific ongoing actions, as granular as different muscle co-contractions of the same forelimb.
