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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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Incentive valence differentially engages open- and closed-loop basal ganglia circuits during movement initiation

This study used neuroimaging to show a ventral putamen-centered open-loop circuit linking emotions and movement in humans. Contextual incentives influence which motor circuit is activated, shedding light on paradoxical kinesia in Parkinson's Disease.

Program: Collaborative Research Network
Team:
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MANUAL CELL COUNTING

MANUAL CELL COUNTING

Program: Collaborative Research Network
Team:
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FISH CODETECTION

DIG and Fluorescein labeled riboprobes Fluorescent in situ hybridization Frozen brain sections

Program: Collaborative Research Network
Team:
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Solutions used for FISH Codetection

Protocol to make the solutions used in the protocol published by AWM lab for FISH Codetection

Program: Collaborative Research Network
Team:
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Selective loss of Primary Cilia and Neurotrophic Signaling in G51D α-Synuclein Mice Highlights a Common Pathway to Parkinson’s Disease

G51D α-synuclein mice mimic disease symptoms, showing cilia loss in specific neurons and impaired neurotrophic signaling, contributing to disease progression. This highlights the role of ciliary dysfunction in Parkinson’s.

Program: Collaborative Research Network
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Elevated phosphorylated α-synuclein and phosphorylated tau in Lrrk2 p.G2019S-mutant mice following influenza A pneumonitis

Influenza virus infection does not alter acute sickness in mice with Lrrk2 mutations. Surviving Lrrk2 p.G2019S KI mice, however, had elevated oxidative stress and phosphorylated a-synuclein and tau proteins in their brains six weeks post-infection.

Program: Collaborative Research Network
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Integrated Representations of Threat and Controllability in the Lateral Frontal Pole

Emotions can strongly influence behavior, as seen in PD paradoxical kinesia. Here, we demonstrate that anticipating threats enhances motor accuracy through interactions between the amygdala and the anterior pole of the lateral prefrontal cortex.

Program: Collaborative Research Network
Team:
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ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis

Polyamines are crucial for brain function. ATP13A4 is the main polyamine transporter in astrocytes, impacting astrocyte morphology, synapse formation, and neurodevelopment. Mutations in ATP13A4 are linked to neurodevelopmental disorders.

Program: Collaborative Research Network
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State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson’s disease

LID is poorly understood, our research on dyskinetic mice show SPNs' properties oscillate during LID and are influenced by dopamine and acetylcholine signaling. Targeting M1 receptors in iSPNs reduced LID severity and improved levodopa effects.

Program: Collaborative Research Network
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Data and Images for Tonic dendritic GABA release by substantia nigra dopaminergic neurons

Data and Images for Tonic dendritic GABA release by substantia nigra dopaminergic neurons

Program: Collaborative Research Network
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Astrocytes mediate the dopaminergic modulation of tonic GABAergic signaling in substantia nigra

To characterize the actions of dopamine on substantia nigra pars reticulata (SNr) GABAergic neurons, optogenetic and electrophysiological tools were used in ex vivo mouse brain slices to monitor synaptic transmission arising from neurons.

Program: Collaborative Research Network
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Rise-and-fall dynamics reveal a molecular and cellular vulnerability axis in prion-like α-synuclein propagation

This study uses a mathematical model to analyze α-synuclein pathology in a Parkinson’s mouse model. It identifies a low-dimensional vulnerability axis linking regional dynamics to neuronal composition and gene expression.

Program: Collaborative Research Network
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Key Resource Table: Molecular analysis of network vulnerability to α-synuclein pathology reveals PAKs as therapeutic targets for Parkinson’s disease

Key resource table for Molecular analysis of network vulnerability to α-synuclein pathology reveals PAKs as therapeutic targets for Parkinson’s disease

Program: Collaborative Research Network
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5-HT4 Receptor Ligand RS67333 Modulates Striatal Acetylcholine and Dopamine Release via the Inhibition of Acetylcholinesterase

The 5-HT4R agonist RS67333 modulates striatal acetylcholine and dopamine release through acetylcholinesterase inhibition, not 5-HT4R activation, highlighting its potential as an AChE inhibitor for brain disorders.

Program: Collaborative Research Network
Team:
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Datasets and Key Resources Table used in Qiao, Q. et al. (2026) 5-HT4 Receptor Ligand RS67333 Modulates Striatal Acetylcholine and Dopamine Release via the Inhibition of Acetylcholinesterase

This repository contains: 1) Key Resources Table containing details on key resources and the persistent identifiers for protocols and code used and generated in this study; 2) Source Data; and 3) README file.

Program: Collaborative Research Network
Team:
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Aligning Science Across Parkinson's
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