DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for Creutzfeldt Jacob Disease — screening already-approved drugs against its 6-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCreutzfeldt Jacob Disease maps to a 6-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 creutzfeldt jacob disease 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
ATP binding cassette subfamily B member 6 (LAN blood group) (ABCB6) — ABCB6 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 y01drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9DBQ · 2.9 Å · ligand CHOLESTEROL HEMISUCCINATE (Y01). Experimental structure, not a prediction.
What the evidence adds up to
A 2006 genotype analysis of appendix tissue samples found prion proteins in two samples from individuals with the homozygous valine (VV) genotype. Before this, all clinical cases of variant Creutzfeldt-Jakob disease had occurred in people with the MM genotype, and only one infection without clinical disease had been identified in a person with the heterozygous MV genotype. The authors note that 60% of people have non-MM genotypes, and raise the possibility that these individuals might be at risk of developing the condition with longer incubation periods, or might be asymptomatic carriers. The study provides no clinical evidence of vCJD in the two people whose tissue harboured prion proteins, and no evidence that their tissue could transmit the disease to others. As of 2006, there were 161 definite or probable vCJD cases in the United Kingdom, far below early model predictions of up to 136,000 cases.
A 1977 report describes two cases of Creutzfeldt-Jakob disease where serial computed tomography of the brain showed rapidly progressive atrophic changes, which the authors state are highly suggestive of the disease. A 2008 study of one brain biopsy compared histochemical and electron-microscopic findings and concluded that histochemical changes in neuronal cytoplasm precede morphological alterations seen under electron microscopy, suggesting that neuronal enzymatic failure explains the clinical picture. A 2016 case report describes a patient whose symptoms resembled corticobasal degeneration but who was later diagnosed with CJD at follow-up. A 2019 case report describes a 68-year-old man who presented with paraparesis, was diagnosed with CJD, and died within one month of diagnosis.
No drug treatment is mentioned in any of these abstracts. No trial of any therapeutic agent is reported. The abstracts describe diagnostic imaging, histopathology, genotype surveillance, and clinical case descriptions, but contain no data on survival extension, symptom modification, or disease reversal from any intervention.
What is still missing is any clinical trial testing a candidate drug for CJD, any funding for such a trial, and any patient stratification strategy that might identify which genetic subgroups could be enrolled. The 2006 genotype finding raises the possibility of asymptomatic carriers, but no screening programme or prophylactic approach has been tested.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
BMJ · 2006 · 27 citations
A new human genotype prone to variant Creutzfeldt-Jakob disease
AbstractFrom the initial discovery of variant Creutzfeldt-Jacob disease (vCJD) in the United Kingdom a decade ago, there has been concern about the ultimate extent and magnitude of the epidemic.1 Early estimates varied widely, with one model predicting up to 136 000 cases.2 Fortunately, the magnitude of the epidemic at present seems to match the lower limit of the early estimates, with 161 definite or probable cases in the United Kingdom. However, the article by Ironside and colleagues on p 1186 may rekindle fears that a larger epidemic is an ongoing threat.3
The study reports a genotype analysis that identified the presence of the homozygous valine (VV) genotype in two samples of appendix tissue that harboured prion proteins. The implication of this finding of most concern is that it raises the possibility that ongoing iatrogenic transmission of vCJD may sustain the epidemic.
Why are the findings from this study worrisome? The current estimates of the prevalence of vCJD have primarily been restricted to populations with one specific genotype (MM), and all clinical cases have occurred in these individuals. This study is the first report of infection in individuals with the VV genotype. One case of infection, but not clinical disease, had been identified in one person with a heterozygous genotype (MV).4 The fear is that the 60% of people with non-MM genotypes may be at risk of developing the condition, possibly with longer incubation periods.5 Alternatively, these people may be asymptomatic carriers who might transmit the condition to other susceptible individuals.
It is important to be cautious in interpreting the results of this study. The study shows the existence of the prion protein in two tissue samples, not clinical evidence of vCJD in two patients. The study also provides no evidence to suggest that tissue from these two people could transmit vCJD to others.
Journal of Computer Assisted Tomography · 1977 · 27 citations
Computed Tomography in the Diagnosis of Creutzfeldt-Jacob Disease
AbstractCreutzfeldt-Jacob disease manifests clinically as a form of presenile dementia. It is now known to be caused by a transmissible agent, probably a "slow virus". Rapidly progressive atrophic changes on serial computed tomograms of the brain are highly suggestive of the disease. Neuroradiographic and pathological findings in two cases of Creutzfeldt-Jacob disease are documented.
Creutzfeldt-Jacob Disease: A Comparative Light-Microscopic, Histochemical and Electron-Microscopic Study
AbstractThe morphological and histochemical findings in a brain biopsy of a case of Creutzfeldt-Jacob disease are compared. The histochemical changes in the cytoplasm of the neurons precede the morphological alterations found with the electron microscope. In this way the neuronal enzymatic failure can explain the clinical picture of this disease.
Journal of Neurology and Neuroscience · 2016 · 2 citations · open access
Sporadic Creutzfeldt-Jacob Disease Presenting With Symptoms of Corticobasal Degeneration: A Case Report
AbstractCreutzfeldt–Jacob disease (CJD) is a rare neurodegenerative disease with a rapid progressive course. Clinically, general symptoms include progressive dementia, ataxia, myoclonus and akinetic mutism, in addition to other presentations such as alien hand. Here, we describe a patient with symptoms resembling corticobasal degeneration (CBD) who was diagnosed with CJD at follow up.
BOĞAZİÇİ TIP DERGİSİ · 2019 · 0 citations · open access
PARAPAREZİ İLE PREZENTE OLAN CREUTZFELDT JACOB HASTALIĞI: OLGU SUNUMU
AbstractCreutzfeldt's Jacob Disease (CJD) is a rare, rapidly progressive, usually fatal neurodegenerative disease that may be caused by a prion protein and transmittable. Patients may present with different clinical features. We report here a 68-year-old man who was admitted to neurology clinic with paraparesis, diagnosed CJD and died within 1 month after diagnosis.
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.
