DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for complex partial epilepsy — screening already-approved drugs against its 44-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleComplex partial epilepsy maps to a 44-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 complex partial epilepsy 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
sodium voltage-gated channel alpha subunit 9 (SCN9A) — SCN9A 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 rdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7W9K · 2.2 Å · ligand O-[(R)-{[(2R)-2,3-bis(octadecanoyloxy)propyl]oxy}(hydroxy)phosphoryl]-L-serine (P5S). Experimental structure, not a prediction.
What the evidence adds up to
Twenty patients with complex partial status epilepticus were identified retrospectively from a specialist neurology hospital. Seventeen experienced recurrent episodes, often at regular intervals over many years, while being treated with effective anti-epileptic drugs. No unifying cause for the recurrences and no common epilepsy aetiologies were identified. Despite the frequency of recurrence and length of history, none of the patients showed marked evidence of cognitive or neurological deterioration. The authors concluded that complex partial status epilepticus is more common than generally recognised, should be differentiated from other forms of non-convulsive status, and is often difficult to treat.
One case report describes a child who developed complex partial status epilepticus after resection of a craniopharyngioma, manifested by confusion and documented by continuous focal seizure patterns in the right temporal region. Another case describes a 14-year-old girl with complex partial seizures since age 10 who developed complex partial status epilepticus, probably because she was not adherent to treatment. During the status epilepticus she received diazepam and phenytoin and became free of seizures after five minutes; the ictal EEG showed spikes and slow waves over the right temporal region.
Approximately 40% of epilepsy has a complex genetic basis with an unknown number of susceptibility genes. The effect of each susceptibility gene acting alone is insufficient to account for seizure phenotypes, but certain numbers or combinations of variations are predicted to raise neuronal hyperexcitability above a seizure threshold. The genetic architecture so far emerging is consistent with a polygenic heterogeneity model. The classification of seizures and epilepsy syndromes, based on the International League Against Epilepsy's systems from 1981 and 1989, distinguishes focal from generalised seizures and remains in clinical use.
What is still missing is a clear understanding of the genetic and environmental factors that drive recurrence in complex partial status epilepticus, and prospective studies large enough to stratify patients by aetiology or genetic susceptibility. No randomised controlled trials of treatment for this specific condition are reported in these abstracts, and the evidence base remains limited to small retrospective series and single case reports.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Journal of Neurology Neurosurgery & Psychiatry · 1994 · 107 citations · open access
Complex partial status epilepticus: a recurrent problem.
AbstractTwenty patients with complex partial status epilepticus were identified retrospectively from a specialist neurology hospital. Seventeen patients experienced recurrent episodes of complex partial status epilepticus, often occurring at regular intervals, usually over many years, and while being treated with effective anti-epileptic drugs. No unifying cause for the recurrences, and no common epilepsy aetiologies, were identified. In spite of the frequency of recurrence and length of history, none of the patients showed any marked evidence of cognitive or neurological deterioration. Complex partial status epilepticus is more common than is generally recognised, should be differentiated from other forms of non-convulsive status, and is often difficult to treat.
AbstractA child had complex partial status epilepticus after resection of a craniopharyngioma. The status epilepticus was manifested by confusion and documented electroencephalographically by continuous focal seizure patterns in the right temporal region. Complex partial status epilepticus is an electroclinical syndrome of prolonged or repetitive complex partial seizures (with continuous interictal confusion) accompanied by electroencephalographic seizure patterns, which are either focal (usually temporal lobe) or secondarily generalized from a focal pacemaker.
A polygenic heterogeneity model for common epilepsies with complex genetics
AbstractApproximately 40% of epilepsy has a complex genetic basis with an unknown number of susceptibility genes. The effect of each susceptibility gene acting alone is insufficient to account for seizure phenotypes, but certain numbers or combinations of variations in susceptibility genes are predicted to raise the level of neuronal hyperexcitability above a seizure threshold for a given individual in a given environment. Identities of susceptibility genes are beginning to be determined, initially by translation of knowledge gained from gene discovery in the monogenic epilepsies. This entrée into idiopathic epilepsies with complex genetics has led to the experimental validation of susceptibility variants in the first few susceptibility genes. The genetic architecture so far emerging from these results is consistent with what we have designated as a polygenic heterogeneity model for the epilepsies with complex genetics.
CONTINUUM Lifelong Learning in Neurology · 2010 · 11 citations · open access
THE CLASSIFICATION OF SEIZURES AND EPILEPSY SYNDROMES
AbstractThis chapter focuses on the classification of seizures and epilepsy syndromes based on the International League Against Epilepsy's classification systems from 1981 and 1989, respectively, which are still used today in clinical practice and have formed the basis for a worldwide standardized approach to diagnosing, treating, and studying seizure disorders. This classification system is based on clinical seizure semiology and EEG correlation and makes a distinction between focal and generalized seizures. The clinical semiology and localization of simple partial, complex partial, and generalized seizures are discussed. Some common partial and generalized epilepsy syndromes are also highlighted.
Arquivos de Neuro-Psiquiatria · 1995 · 1 citations · open access
Complex partial status epilepticus in a child
AbstractComplex partial status epilepticus (SE) has been reported rarely in children. We describe the clinical case of a 14 year-old girl with complex partial seizures (CPS) since age 10 who developed a complex partial SE probably because she was not adherent to treatment. The neurologic examination and computed tomography scan were normal. During the SE she received diazepam and phenytoin and became free of the seizures after 5 minutes. The ictal EEG showed spikes and slow waves over the right temporal region.
Oxford University Press eBooks · 2018 · 0 citations
Seizures
AbstractSeizures are transient neurological events caused by abnormal excessive or synchronous neuronal activity in the brain. This can arise from a localized brain region, causing focal seizures, or simultaneously from both hemispheres, leading to generalized seizures. Epilepsy is the tendency to develop recurrent seizures and is usually diagnosed after two or more unprovoked seizures. This chapter covers simple partial seizures (sometimes called aura), complex partial seizures, and focal (or partial) seizures, their differential diagnosis, context, approach to diagnosis, key diagnostic tests, therapy, and prognosis, as well as dealing with uncertainty in a 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.
