DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for central nervous system origin vertigo — screening already-approved drugs against its 2-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCentral nervous system origin vertigo maps to a 2-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 central nervous system origin vertigo 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
In a 1991 statistical analysis of 140 patients presenting with vertigo and dizziness, only 6.4% were classified as central nervous system origin. The largest group was peripheral origin at 62.1%, followed by unknown origin at 21.4% and other causes at 10%. The most common single diagnosis was benign paroxysmal positional vertigo. A 2006 review notes that several vertigo syndromes are now known to be familial, with susceptibility loci and mutations identified, but genetic heterogeneity is common and much remains unknown about pathophysiology and treatment.
A 1972 symposium states that vertigo can be caused by lesions at many locations in the central nervous system, and that such lesions should be diagnosed and treated by a neurologist. A 2025 review reports that otogenic vertigo accounts for approximately 70% of all vertigo and severely affects quality of life, and that neuroimaging techniques are providing new insights into central nervous mechanisms, but this is a review of imaging evidence, not a treatment trial.
A 2000 study in humans found that vestibular caloric stimulation, which clinically produces vertigo, inhibits noradrenaline neurons in the locus coeruleus. The authors suggest this inhibition is involved in the development of vertigo and may also contribute to drowsiness and sensory mismatch. They note that the cholinergic neuron system may mediate this inhibition, and that the histaminergic system appears to be independent. No drug was tested in this study.
No clinical trial data exist for any drug specifically for central nervous system origin vertigo. What is missing is any randomised controlled trial that separates central from peripheral vertigo, a validated biomarker or imaging protocol to stratify patients by central cause, and funding for such a trial.
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 · 9 citations
The Genetics of Vertigo
AbstractVertigo is a common principal complaint among patients seen by primary care physicians, neurologists, and otolaryngologists. The most common causes of recurrent episodes of vertigo are benign inner ear disorders, but central nervous system disorders must be excluded. Several common vertigo syndromes are now known to be familial, a feature distinguishing them from other common causes of vertigo. Familial vertigo has been recognized in patients with isolated recurrent attacks of vertigo, genetic deafness syndromes, and in patients with neurological disorders. Although susceptibility loci and mutations have been identified, genetic heterogeneity is common in all familial vertigo syndromes. Research in these disorders has advanced the understanding of vertigo pathophysiology but much remains to be known. This article provides an overview of the clinical features, genetic analyses, and treatment strategies for these disorders.
Practica Oto-Rhino-Laryngologica · 1991 · 2 citations · open access
Patients with vertigo seen in our clinic; A statistical analysis.
AbstractA statistical analysis was conducted on 140 patients (48 males, 92 females) who visited our clinic complaining of vertigo and dizziness from June 1989 to March 1990. Vertigo and dizziness of peripheral origin accounted for 62.1%, of central origin 6.4%, others 10%, and of unknown origin 21.4%. BPPV (Benign Paroxysmal Positional Vertigo) was the most common type of vertigo seen in our clinic. In the 30 patients with disease of unknown origin (21.4%), we analyzed the reasons that we could not diagnose them and tried to classify them from the viewpoint of patterns of onset.
Equilibrium Research · 2000 · 2 citations · open access
Vestibulo-Autonomic Reflex and Monoamines.
AbstractYates has reported that serotonin neurons in the raphe nuclei are associated with vestibulo-sympathetic responses and may possibly control BP changes during body replacement. Pompeiano demonstrated that the noradrenaline (NA) neurons in the locus coeruleus (LC) participate in posture control and modify the vestibulo-spinal reflex.In our studies, LC-NA neuronal activity was inhibited by vestibular caloric stimulation, which causes vertigo clinically in humans. The vestibular input may be modified by the ventrolateral medulla (VLM) and then inhibit LC neuronal activity via GABAA receptors. Simultaneously, the VLM, the cardiovascular center in the brainstem, may change BP during vestibular stimulation. Thus, it is suggested that LC-NA inhibition is involved in the development of vertigo. Moreover, it is speculated that sopite syndrome, one of the major symptom complexes of motion sickness, is also evoked by LC-NA inhibition.The central LC-NA and cholinergic neuron systems participate in vertigo and motion sickness, independent of the histaminergic neuron system. On the other hand, the cholinergic neuron system may mediate LC-NA inhibition during vestibulo-autonomic responses.The LC-NA system projects to most higher centers and affects sensory information processing. Therefore, it is suggested that the suppression of the sensory information processing induced by LC-NA inhibition causes drowsiness, one of the major symptoms of vertigo and motion sickness. It is also speculated that LC-NA inhibition participates in the development of sensory mismatch.
Symposium on ear diseases. II. Vestibular evaluation and the brain stem
AbstractAbstract Vertigo can be caused by many lesions at many locations both in the peripheral organ and in the central nervous system. The lesions occurring in the central nervous system should be diagnosed and treated by a neurologist, but the otolaryngologist can be of great assistance through the study of the VIIIth cranial nerve function and its connections with the oculomotor system. As examples, four different brain stem syndromes are mentioned. (These were illustrated by movies at the meeting.)
DOAJ (DOAJ: Directory of Open Access Journals) · 2025 · 0 citations · open access
Neuroimaging progress of otogenic vertigo
AbstractThe incidence of otogenic vertigo accounts for approximately 70% of all vertigo, presenting a sensation of surrounding objects moving and balance disturbances, accompanied by nausea, vomiting, and emotional changes, severely affecting quality of life in patients. Neuroimaging techniques have been widely used to observe structural and functional changes in related brain regions, and provide new insights into the mechanisms of vertigo. This paper aims to review the recent neuroimaging advancements in the study of central nervous mechanisms of otogenic vertigo, offering a imaging evidence for further exploration of related neuropathological mechanisms of otogenic vertigo.
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.
