Experiments
Searchable full-text extractions: founding hypothesis, core claims, experimental setups, key results and statistics — pulled out of each paper as structure. Search a cell line, an assay or an entity (e.g. HUH7) and find every paper that worked with it. This corpus stands on its own: most entries carry no reproduction assessment (yet).
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Has reproduction · 55
Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson's disease.
PMID 38566100 · PMC10985960 · Cell communication and signaling : CCS · 2024 · 8 claims · 8 setups
Microglia, endothelial cells, and pericytes exhibit the highest type I interferon (IFN-I) activity among PD midbrain cell types, with microglia showing markedly higher activity in PD.
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Has reproduction · 70
Spatial transcriptomics reveals the molecular signatures of prodromal and advanced α-synucleinopathy.
PMID 41736854 · PMC12927100 · iScience · 2026 · 8 claims · 6 setups
Induction of aSyn pathology in rodent brainstem at the early/prodromal stage triggers upregulation of energy metabolism pathways (glycolysis, oxidative phosphorylation, fatty acid metabolism)
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Neurofibrillary tau pathology modulated by genetic variation of alpha-synuclein.
PMID 18661559 · PMC8957216 · Annals of neurology · 2008 · 7 claims · 5 setups
The SNCA intron 4 marker rs2572324 is associated with the extent of neurofibrillary tangle (Braak stage) pathology.
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Early onset familial Alzheimer Disease with spastic paraparesis, dysarthria, and seizures and N135S mutation in PSEN1.
PMID 18580586 · PMC2750842 · Alzheimer disease and associated disorders · 2008 · 8 claims · 8 setups
The PSEN1 N135S mutation causes EOFAD with an atypical phenotype including spastic dysarthria, limb spasticity, and seizures in addition to typical cognitive deficits
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Genomic views of distant-acting enhancers.
PMID 19741700 · PMC2923221 · Nature · 2009 · 8 claims · 8 setups
Meta-analysis of ~1200 top GWAS SNPs found that in 40% of cases (472/1170) no known exons overlap the linked SNP or its haplotype block, implying noncoding variation causally contributes to many traits.