DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for progressive supranuclear palsy — screening already-approved drugs against its 34-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleProgressive supranuclear palsy maps to a 34-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for progressive supranuclear palsy is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
eukaryotic translation initiation factor 2 alpha kinase 3 (EIF2AK3) — EIF2AK3 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet methylaminodrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4X7K · 1.8 Å · ligand 4-{2-amino-3-[5-fluoro-2-(methylamino)quinazolin-6-yl]-4-methylbenzoyl}-1-methyl-2,5-diphenyl-1,2-dihydro-3H-pyrazol-3-one (3Z3). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Opinion in Neurology · 1997 · 22 citations
The clinical and pathologic hallmarks of progressive supranuclear palsy
AbstractThis article reviews recent studies evaluating the clinicopathologic markers of progressive supranuclear palsy, which have helped establish standardized clinical and pathologic diagnostic criteria. Although these criteria increase diagnostic accuracy, the clinical and pathologic overlap between progressive supranuclear palsy and other disorders remains. Factors that may contribute toward managing progressive supranuclear palsy patients better are discussed and the etiopathogenicity of the disorder is hypothesized.
Current Opinion in Neurology · 2002 · 22 citations
Progressive supranuclear palsy: clinical and genetic aspects
AbstractPURPOSE OF THE REVIEW: This review focuses on the recent additions to the literature in the clinical and genetic aspects of progressive supranuclear palsy. RECENT FINDINGS: Clinical features of progressive supranuclear palsy are reasonably well established and known to be quite characteristic. Recent epidemiological studies suggest that the disorder is more common than previously considered and that it is frequently misdiagnosed. New laboratory and novel imaging techniques are being tested and cerebrospinal fluid levels of tau protein have been found helpful in diagnosis. Pathological and biochemical studies in progressive supranuclear palsy brains have shown the predominance of hyperphosphorylated tau isoforms which contain the sequence encoded by exon 10 (4R) aggregated into filaments. Familial tauopathies linked to tau gene mutations showing clinical and neuropathological overlap with sporadic progressive supranuclear palsy have been described. Despite recent discoveries of the strong genetic association of sporadic progressive supranuclear palsy with tau gene polymorphisms, a specific risk allele for developing the palsy has not yet been identified yet. SUMMARY: Recent clinical studies and clinicopathological correlations are contributing significantly to the delineation of the clinical features of progressive supranuclear palsy. These features and the appropriate use of laboratory tests allow for an earlier identification of the disease and a more accurate premortem diagnosis. However, no specific biological markers for the disorder are available yet, and consequently diagnosis in the early stages or when some of the characteristic signs and symptoms are missing, remains a major challenge. Despite the recent advances in the understanding of genetic factors involved in progressive supranuclear palsy, the cause of the disease still remains unknown. Biochemical studies in brains from progressive supranuclear palsy patients provide a potential helpful instrument to improve the characterization of this disorder.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
