DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for migraine, familial hemiplegic, 2 — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMigraine, familial hemiplegic, 2 maps to a 1-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 migraine, familial hemiplegic, 2 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.
What the evidence adds up to
Hemiplegic migraine is a rare subtype of migraine with aura that includes transient hemiplegia caused by motor aura. It occurs in either a sporadic or familial form, distinguished only by family history. Treatment trials are anecdotal, though verapamil and acetazolamide have shown promise in these limited reports. By definition the neurological impairments are reversible, but a few cases of permanent deficits have been reported, leading some authors to suggest aggressive prophylactic therapy for patients with recurrent attacks. One case describes a sporadic hemiplegic migraine patient with unusually prolonged deficit and progression to quadriplegia who returned to baseline seven days after onset; diffusion-weighted imaging helped exclude infarction.
The familial form, familial hemiplegic migraine type I, is a rare hereditary subtype with autosomal dominant inheritance. Molecular mechanisms of migraine attack remain unclear, but constructed hypothetical signalling pathways have been used to identify key molecules and pathways for further experimental and clinical studies. The clinical characteristics of 105 patients with sporadic hemiplegic migraine have been compared with those of patients with migraine with typical aura and patients with familial hemiplegic migraine in a study at the Danish Headache Center.
Seven loci with significant linkage to migraine with or without aura have been identified on chromosomes 1q31, 4q24, 6p12.2-21.1, 11q24, 14q21.2-q22.3, 15q11-q13 and Xq24-28, suggesting migraine susceptibility genes in these regions. Identification of genes predisposing to the more common and genetically complex forms of migraine has been complicated by clinical and genetic heterogeneity. The major challenge remains the identification of disease-susceptibility genes and understanding how migraine risk is influenced by the interaction of these variants with each other and with specific environmental factors.
What is still missing are properly powered randomised controlled trials for any prophylactic agent in hemiplegic migraine, including verapamil and acetazolamide. The anecdotal treatment evidence cannot support a recommendation. Patient stratification by genetic subtype is not yet standard, and no trial has been designed to test whether the molecular pathways identified in familial hemiplegic migraine type I translate to effective treatments for either familial or sporadic forms.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Seminars in Neurology · 2006 · 48 citations
Sporadic and Familial Hemiplegic Migraine: Diagnosis and Treatment
AbstractHemiplegic migraine is a rare subtype of migraine with aura associated with transient hemiplegia. The weakness is caused by motor aura. Hemiplegic migraine is the only headache syndrome associated with known genetic mutations and serves as a model for understanding more common varieties of migraine. Because the phenotype includes striking yet transient neurological signs and symptoms, it is imperative that clinicians know the differential diagnosis to rule out possible secondary etiologies when treating patients with hemiplegic spells. Hemiplegic migraine occurs with equal prevalence in either a sporadic or familial form differentiated only by family history. Thus far, treatment trials are anecdotal, although verapamil and acetazolamide have shown promise.
Headache The Journal of Head and Face Pain · 2013 · 20 citations · open access
Sporadic Hemiplegic Migraine With Permanent Neurological Deficits
AbstractBy definition, the neurologic impairments of hemiplegic migraine are reversible. However, a few cases of permanent neurologic deficits associated with hemiplegic migraine have been reported. Herein, we present the case of a patient with permanent impairments because of hemiplegic migraine despite normalization of associated brain magnetic resonance imaging abnormalities. Cases like these suggest the need to consider aggressive prophylactic therapy for patients with recurrent hemiplegic migraine attacks.
Headache The Journal of Head and Face Pain · 1986 · 8 citations
Familial Hemiplegic Migraine: A New Case
AbstractSYNOPSIS The definition of familial hemiplegic migraine is still unsettled. We report the case of a young man who has had hemiplegic migraine attacks for ten years. CT of the brain was abnormal with a low density in the temporal lobe, suggesting infarction and probably having no relation to the attacks. There was a clear family history of hemiplegic migraine, possibly with the same type of attack. Ergotamine tartrate seemed to be effective in preventing headache. This case challenges the current clinical definition of familial hemiplegic migraine, in that while the attack pattern was hereditary, the hemiplegia occurred as an aura rather than accompanying and outlasting the headache.
Journal of Neurology & Stroke · 2017 · 2 citations
Familial Hemiplegic Migraine Type I: The Molecular Signaling Pathway
AbstractMigraine is a multifactorial disease, manifested by intense bouts of recurrent headaches.Molecular mechanisms of migraine attack are not clear.In this study, we carried out the analysis of molecular processes in the pathogenesis of a rare hereditary form of migrainefamilial hemiplegic migraine type I. Constructed hypothetical signaling pathways allowed us to understand the causes of a migraine attack and identify key molecules and signaling pathways for further experimental and clinical studies.
The Molecular Genetics of Migraine: Toward the Identification of Responsible Genes
AbstractMigraine is a complex debilitating neurovascular disease affecting approximately 15% of the Western populations. Familial clustering, twin studies and segregation analyses suggest that migraine has a significant genetic component, but the number of genes involved remains unclear. The progress in migraine genetics has recently jumped ahead with the identification of genes responsible for Familiar Hemiplegic Migraine (FHM), a rare subtype of migraine with aura showing autosomal dominant mode of inheritance. Nevertheless, the knowledge about common types of migraine has been particularly rewarding and recently, seven loci with significant linkage to migraine with or without aura have been identified on 1q31, 4q24, 6p12.2-21.1, 11q24, 14q21.2-q22.3, 15q11-q13 and Xq24-28, suggesting the presence of migraine susceptibility genes in these regions. Identification of genes predisposing to the more common and genetically complex forms of migraine has been complicated by clinical and genetic heterogeneity of the disease. The major challenge in the coming years facing biomedical research of migraine is the identification of disease-susceptibility genes and the understanding of how migraine risk can be influenced by the interaction of these variants with each other and with specific environmental factors in order to provide individuals with clinically-useful diagnostic, prognostic and therapeutic information. This paper briefly summarizes the previous knowledge and highlights some recent developments in the complex genetic nature of migraine. Keywords: Familial hemiplegic migraine, migraine with aura, migraine without aura
Galter Health Sciences Library, Northwestern University · 2003 · 0 citations · open access
Sporadic Hemiplegic Migraine: A Separate Entity
AbstractThe clinical characteristics of 105 patients with sporadic hemiplegic migraine (SHM) were compared with those of patients with migraine with typical aura (MA) and patients with familial hemiplegic migraine (FHM) in a study at the Danish Headache Center, Glostrup Hospital, Gentofte Hospital, University of Copenhagen, and the John F Kennedy Institute, Denmark.
AbstractHemiplegic migraine is a rare form of migraine variant. It is characterized by recurrent attacks of headache associated with temporary neurological deficit, usually unilateral hemiparesis or hemiplegia. It can be difficult to distinguish from migrainous stroke clinically, and a full neurological work-up and careful review of medical history and symptoms are necessary for the diagnosis. Two forms of hemiplegic migraine are known: familial and sporadic, phenotypically similar, differentiated by the absence of family history of similar attacks in the sporadic form. We report a case of sporadic hemiplegic migraine with unusually prolonged deficit and progression to quadriplegia with complete return to baseline 7 days after onset. Diffusion weighted images helped in excluding infarction.
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.
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