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Output Catalog

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 created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.

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Single cell eQTL mapping reveals convergent glial–neuronal risk architecture in Parkinson’s disease

Population-scale, disease-context aware meta single-nucleus eQTLs mapping (N = 1,197) in nine cell types from cortex and substantia nigra identifies 125 risk genes and cell types for PD GWAS signals.

Program: Collaborative Research Network
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MANUAL CELL COUNTING

MANUAL CELL COUNTING

Program: Collaborative Research Network
Team:
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CREsted: modeling genomic and synthetic cell-type-specific enhancers across tissues and species

CREsted, a sequence-based deep learning model, analyzes genomic regulatory code, decodes enhancer grammar, and designs synthetic enhancers. It preprocesses single-cell data, models chromatin accessibility, and compares cell states across tissues.

Program: Collaborative Research Network
Team:
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EnvA-N2c-deltaG-H2B-HA-FlpO

Generated for anatomical anterograde tracing experiments by Columbia University Zuckerman Institute Molecular Tools Core Facility (RRID:SCR_026201).

Program: Collaborative Research Network
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pAAVDJ-Ef1a-FDOI-mScarlet

Generated for anatomical tracing experiments by Columbia University Zuckerman Institute Molecular Tools Core Facility (RRID:SCR_026201).

Program: Collaborative Research Network
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FushikiA_etal_2024: PD Model Mice Study – v1.0 Code

Repository offers tools for processing, analyzing, and visualizing data related to PD and dopaminergic neurons.

Program: Collaborative Research Network
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A druggable ATP13A3–antizyme switch controls adaptive polyamine uptake in cancer

Cellular polyamine depletion for cancer treatment is hindered by compensatory uptake. ATP13A3, not ATP13A2, is the key polyamine importer affected by DFMO. Antizyme inhibits uptake by ATP13A3, suggesting a targetable strategy for cancer therapy.

Program: Collaborative Research Network
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A single Citrobacter rodentium infection in Pink1 knockout and wild type mice leads to regional blood-brain-barrier perturbation and limited microglial activation without dopamine neuron axon terminal loss

Research suggests immune system activation may contribute to Parkinson’s disease development. Mild infections can increase BBB permeability, triggering brain inflammation in genetically susceptible individuals, potentially leading to PD pathology.

Program: Collaborative Research Network
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Dataset for “A single Citrobacter rodentium infection in Pink1 knockout and wild-type mice leads to regional blood-brain-barrier perturbation and limited microglial activation without dopamine neuron axon terminal loss”

Immune system activation may contribute to PD development. Infection increases BBB permeability in mice, leading to brain inflammation. This suggests infections could trigger PD in genetically susceptible individuals.

Program: Collaborative Research Network
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Generation of DATcrePink1 Knockout Mice Expressing tdTomato in Dopaminergic Neurons

Protocol details generation of DATcrePink1 mice expressing tdTomato in dopaminergic neurons. Covers Pink1 KO, HET, WT variants, animal housing, breeding, and genotyping procedures.

Program: Collaborative Research Network
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Semi-automated quantification of microglial CD68 and Iba1 immunohistochemistry signal in mouse brain slices

A standardized method for semi-automated detection and quantification of CD68 and Iba1 in brain sections using image acquisition, AI segmentation, and data analysis.

Program: Collaborative Research Network
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Automated Quantification of Dopaminergic Neurons in Floating Sections V.1

Automated method for detecting and measuring dopaminergic neurons in brain sections using image capture, AI segmentation, and data analysis in SNc and VTA regions.

Program: Collaborative Research Network
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STING dampens the unfolded protein response to enable the presentation of self antigens on MHC-I during inflammation

STING pathway regulates antigen presentation through the UPR, impacting immune response in PD and autoimmune diseases. Targeting STING and UPR could be therapeutic.

Program: Collaborative Research Network
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Dataset for “STING dampens the unfolded protein response to enable the presentation of self-antigens on MHC-I during inflammation”

STING pathway activation impacts antigen presentation through the UPR and may be a target for therapeutic intervention in PD and autoimmune diseases.

Program: Collaborative Research Network
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pBABE-puro-mCHerrry-FTL

Ferritin Light Chain gene (FTL) cloned into pBABE puro-mCherrry-GTW

Program: Collaborative Research Network
View Lab Material
Aligning Science Across Parkinson's
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