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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’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.
results for "studer"
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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.
Induced Pluripotent Stem Cells: A Tool for Modelling Parkinson’s Disease
PD involves loss of dopaminergic neurons in the substantia nigra. Patient-derived iPSC models aid in understanding the disease and identifying potential treatments. More research is needed on age-related aspects and gene-environment interactions.
SARS-CoV-2 infection causes dopaminergic neuron senescence.
The ASAP-supported aspect of this study involves the DA neuron senescence work, and experiments using ASAP lines (isogenic a-SYN triplication) to assess interaction of genetic vulnerability with viral-induced senescence as PD penetrance factor.
Genome-wide CRISPR screen identifies neddylation as a regulator of neuronal aging and AD neurodegeneration.
We found that neddylation-inhibition triggers age-related features in PSC-derived neurons for modeling AD or PD. This strategy can induce late-onset phenotypes including degeneration when applied to DA neurons from PD- versus isogenic control PSCs.
Deep sequencing of proteotoxicity modifier genes uncovers a Presenilin-2/beta-amyloid-actin genetic risk module shared among alpha-synucleinopathies
The authors study patients based on protein aggregation phenotype to detect variants in a targeted set of genes.
The SATB1-MIR22-GBA axis mediates glucocerebroside accumulation inducing a cellular senescence-like phenotype in dopaminergic neurons
Study shows SATB1, MIR22HG, and GBA genes form a pathway in Parkinson's Disease. Dysregulation leads to GluCer accumulation, causing cellular senescence in dopaminergic neurons, potentially explaining neuroinflammation seen in PD and aging.
TNF-NF-κB-p53 axis restricts in vivo survival of hPSC-derived dopamine neurons
The ASAP-related findings are the DA neuron purification strategy developed (CD49e-/CD184+) developed and validated in this manuscript, which is suitable for PD-iPSC based disease modeling and DA-neuron related CRISPR screens from our consortium.