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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Proteomics for STING KO and STINGRRAA RAW 264.7 macrophages
Using immunopeptidomics analysis we showed that STING regulates the repertoire of peptides displayed at the cell surface of macrophages during inflammation, highlighting a potential role in immunosurveillance and potential targets for therapy
Code used in “Lrrk2 G2019S mutation incites increased cell-intrinsic neutrophil effector functions and intestinal inflammation in a model of infectious colitis”
Using scRNAseq and flow cytometry, we demonstrated that the Lrrk2-G2019S mutation is associated with an increased neutrophil presence in the colonic lamina propria, Th17 skewing, upregulated Il17a, and greater colonic pathology during infection.
Transcriptomic analysis of colonic lamina propria cells in LRRK2 G2019S mice compared to wild type following intestinal microbial infection
Using scRNAseq and flow cytometry, we demonstrated that the Lrrk2 G2019S mutation is associated with an increased neutrophil presence in the colonic lamina propria during infection and a Th17 skewing, upregulated Il17a, and greater colonic…
Microbes and Parkinson’s Disease: from associations to mechanisms
Several microbes, including viruses, bacteria, and fungi, have been associated with an increased risk of PD in humans. Microbial infections can induce similar common pathways that are associated with PD, including systemic inflammatory responses,…
LRRK2 regulates the activation of the unfolded protein response and antigen presentation in macrophages during inflammation
Absence of PINK1 leads to MitAP over-activation engaging autoimmune mechanisms. This pathway is induced by TLR4, cGAS-STING, and UPR activation in response to inflammatory signals. LRRK2 and STING regulate transition from innate to adaptive immunity
Protocols for “Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice”
This is a collection of protocols for the manuscript “Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice”
Mitochondrial Antigen Presentation in RAW macrophages
This protocol details methods for 3-day Mitochondrial Antigen Presentation Assay in a murine macrophage cell line (RAW) that expresses a glycoprotein B (gB) of herpes simplex virus 1 (HSV1) targeted to the mitochondrial matrix (mito-gB). A…
Protocols for “Characterizing the diversity of enteric neurons using Dopamine Transporter (DAT)-Cre reporter mice”.
This is a collection of protocols associated to the manuscript “Characterizing the diversity of enteric neurons using Dopamine Transporter (DAT)-Cre reporter mice”.
Synaptotagmin-1-dependent phasic axonal dopamine release is dispensable for basic motor behaviors in mice
In Parkinson’s disease (PD), motor dysfunctions only become apparent after extensive loss of DA innervation. This resilience has been hypothesized to be due to the ability of many motor behaviors to be sustained through a diffuse basal tone of DA;…
Single cell transcriptomics from DAT-Cre mouse gut tissue
Colonic myenteric cells were dissociated, and live tdTomato-positive cells were FACS-collected. Colons were isolated from 2 male and female wild type adult DAT-Cre mice. Wild type C57Bl6/J was used as control for gating. Cells were processed…
The calcium sensor synaptotagmin-1 is critical for phasic axonal dopamine release in the striatum and mesencephalon, but is dispensable for basic motor behaviors in mice
In this work, we conditionally deleted the calcium sensor synaptotagmin-1 (Syt1) in DA neurons (cKODA mice) to abrogate most activity-dependent axonal DA release in the striatum and mesencephalon. Syt1 cKODA mice showed intact performance in…
MAPL regulates gasdermin-mediated release of mtDNA from lysosomes to drive pyroptotic cell death
These data place mitochondria-to-lysosome transport as a driver of pyroptosis and link multiple PD proteins along a common inflammatory pathway.
Comparative analysis of methods to reduce activation signature gene expression in PBMCs
Preserving the in vivo cell transcriptome is essential for accurate profiling, yet factors during cell isolation including time ex vivo and temperature induce artifactual gene expression, particularly in stress-responsive immune cells. In this…
Modeling gene-environment interactions in Parkinson’s Disease: Helicobacter pylori infection of Pink1-/- mice induces CD8 T cell-dependent motor and cognitive dysfunction.
Here, we demonstrate in a mouse model deficient in the PD-associated gene Pink, that infection with the human PD-associated gastric bacterium Helicobacter pylori leads to development of motor and cognitive signs resembling prodromal features of PD.
Adoptive transfer of mitochondrial antigen-specific CD8+ T-cells in mice causes parkinsonism and compromises the dopamine system
By adoptively transferring mitochondrial peptide-specific CD8+ T cells into WT and PINK1 KO mice, we find that this leads to L-DOPA-reversible motor impairment and to robust loss of DA neurons and axonal markers in the striatum in both PINK KO and WT
