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’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.
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surmeierlab/EZT2022SA: EZTNotebooks
Jupyter Notebooks for Science Advances paper ZampeseSA2022 README (8 AUG 2022): This repository contains five Jupyter Notebooks (Python 3.0) created or modified for specific use with action potential analysis for the Zampese, et.al. 2022 Science…
Day2024 R code and analysis
This script and accompanying folder should reproduce figures 1-4 and supplementary figure S1 of the manuscript in GABAergic regulation of striatal spiny projection neuron excitability depends upon their activity state (2023).
Collection of protocols of Team Deleidi used in the publication: “”LRRK2 kinase activity regulates GCase level and enzymatic activity differently depending on cell type in Parkinson’s disease””
Collection of protocols of Team Deleidi used in the publication: ""LRRK2 kinase activity regulates GCase level and enzymatic activity differently depending on cell type in Parkinson’s disease""
Available ASAP-related hPSC collection from Team Studer
Collection of human pluripotent stem cell lines consisting of isogenic GBA, LRRK2, SNCA series, KI-reporter lines for TOMM20, b-actin, LAMB1, LAMP1, a-synuclein overexpression lines, and other hPSC resources.
Team Science Approaches to Unravel Monogenic Parkinson’s Disease on a Global Scale
In this article, we describe combining both efforts in a merger project resulting in a global monogenic PD cohort with the buildup of a sustainable infrastructure to identify the multi-ancestry spectrum of monogenic PD and enable studies of factors…
State-dependent GABAergic regulation of striatal spiny projection neuron excitability
Synaptic transmission mediated by GABAA receptors (GABAARs) in adult, principal striatal spiny projection neurons (SPNs) can suppress ongoing spiking, but its effect on synaptic integration at sub-threshold membrane potentials is less well…
Day2023 supplementary dataset
Datasets for all supplementary figures S1-4 in GABAergic regulation of striatal spiny projection neuron excitability depends upon their activity state (2023).
Day2023 dataset
Datasets for all figures 1-8 in: GABAergic regulation of striatal spiny projection neuron excitability depends upon their activity state. Image is taken from Fig 1B inset and illustrates RiboTag-eGFP in SPNs of the striatum.
Source data for “Ca2+ channels couple spiking to mitochondrial metabolism in substantia nigra dopaminergic neurons”
Source data for publication: “Ca2+ channels couple spiking to mitochondrial metabolism in substantia nigra dopaminergic neurons”.
Ca2+ channels couple spiking to mitochondrial metabolism in substantia nigra dopaminergic neurons
The authors explore how cellular energy production and demand are matched.
State-dependent GABAergic regulation of striatal spiny projection neuron excitability: NEURON + Python model of striatal projection neurons
This repository contains a NEURON + Python model of striatal projection neurons (or SPNs) designed to simulate the interaction between GABAergic and glutamatergic synaptic inputs.
Tonic dendritic GABA release by substantia nigra dopaminergic neurons
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.
Distributed dopaminergic signaling in the basal ganglia and its relationship to motor disability in Parkinson’s disease
Degeneration of dopaminergic neurons in the brain causes PD motor symptoms. Recent research shows dopamine's role in basal ganglia regions beyond striatum impact movement control. Restoring dopamine signaling outside the striatum can alleviate PD.
α-Synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons at-risk in Parkinson’s disease
Our findings suggest that disruption of mitochondrial function, and the subsequent bioenergetic deficit, is a proximal step in the cascade of events induced by aSYN pathology leading to dysfunction and degeneration of neurons at-risk in PD.
Source data for “Feed-forward metabotropic signaling by Cav1 Ca2+ channels supports pacemaking in pedunculopontine cholinergic neurons”
Source Data and images from the paper: Feed-forward metabotropic signaling by Cav1 Ca2+ channels supports pacemaking in pedunculopontine cholinergic neurons
