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.
-
Output Type
-
Program
-
CRN Team Name
-
Theme
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.
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.
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.
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.
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.
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.
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.
pBABE-puro-mCHerrry-FTL
Ferritin Light Chain gene (FTL) cloned into pBABE puro-mCherrry-GTW
pBABE-puro-mCHerrry-NCOA4
NCOA4 gene cloned into pBABE puro-mCherrry-GTW
Protocols for “LRRK2 mutations block NCOA4 trafficking upon iron overload leading to ferroptotic death”
LRRK2-G2019S affects iron homeostasis in macrophages by dysregulating iron-related proteins. This leads to impaired ferritinophagy, increased oxidative stress, and cell death, highlighting LRRK2's role in iron regulation in Parkinson's Disease.
An LRRK2 variant blocks NCOA4 trafficking upon iron overload, leading to ferroptotic death
We examined the impact of mutant LRRK2-G2019S on iron homeostasis within a model macrophage cell line. Results revealed a dysregulation of iron-related proteins in steady state and a complete block in the degradation of the ferritinophagy NCOA4.
Protocols for “STING dampens the unfolded protein response to enable the presentation of self-antigens on MHC-I during inflammation”
STING pathway regulates MitAP through the UPR, establishing it as a key immune regulator in autoimmunity and PD.
Dataset for “An LRRK2 variant blocks NCOA4 trafficking upon iron overload, leading to ferroptotic death”
LRRK2 as a key regulator of iron homeostasis and point to the need for an increased focus on the mechanisms of iron dysregulation in PD
Proteomics for “An LRRK2 variant blocks NCOA4 trafficking upon iron overload, leading to ferroptotic death”
LRRK2 as a key regulator of iron homeostasis and point to the need for an increased focus on the mechanisms of iron dysregulation in PD
Cell-autonomous and non-cell-autonomous drivers of dopamine neuron vulnerability in Parkinson’s disease
This review examines evidence for cell-autonomous mechanisms and non-cell-autonomous processes arising from glial and peripheral immune cells and how these pathways can converge to create chronic cellular stress and trigger cell death mechanisms.
