DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hearing loss, autosomal dominant 84 — 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 moduleHearing loss, autosomal dominant 84 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 hearing loss, autosomal dominant 84 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
An estimated 6.7% of a UK clinical population and 0.7% of the general population have hearing loss greater than 70 dB averaged over 0.5, 1, and 2 kHz, based on a retrospective study of 32,781 cases from which 2,199 cases of severe or profound loss were identified and a stratified sample of 302 adults was contacted. The study notes this probably underestimates prevalence. Hearing loss affects about 4% of people under 45 years of age. Globally, over 1.5 billion people are affected, with genetic factors accounting for roughly 50% of congenital cases.
Approximately 30% of genetically determined deafness occurs in syndromic form and 70% in nonsyndromic form. The majority of genetic hearing loss shows an autosomal recessive pattern, but autosomal dominant, X-linked, and mitochondrial forms exist. Mutations in GJB2 explain a high proportion of genetic deafness in several populations. Four syndromic forms are described: Jervell and Lange-Nielsen (mutations in KCNQ1, KCNE1), Wolfram (WFS1), branchio-otorenal (EYA1, SIX1), and Alport (COL4A3, COL4A4, COL4A5). Mitochondrial DNA mutations also contribute.
No specific drug treatment for autosomal dominant hearing loss is mentioned in any of these abstracts. The 1978 symposium states that definitive therapy is often lacking, and management focuses on prevention of progression when possible, recognition of associated disorders, compensation for disability, and rehabilitation. The 2025 collection includes papers on gene therapy and basic mechanisms of protection, but no drug is named or tested in the provided abstracts. The 1991 paper (title in Spanish) confirms the complex genetic landscape and the limitations of whole-exome sequencing in achieving a 100% diagnostic rate due to genetic heterogeneity.
What is still missing is a specific drug candidate for autosomal dominant hearing loss 84, any clinical trial testing a repurposed drug for this condition, and patient stratification by the causative gene mutation. The abstracts provide no efficacy data for any pharmacological intervention in this disease.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
International Journal of Audiology · 2012 · 32 citations
Prevalence & characteristics of severe and profound hearing loss in adults in a UK National Health Service clinic
AbstractLaura Turton*ab & Pauline Smithcda Hearing Link, Eastbourne, UKb The Centre for Hearing & Balance Disorders, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UKc Hearing Services Department, University Hospitals of Leicester NHS Trust, Leicester, UKd Medical Research Council Hearing and Communication Group, Royal Free London NHS Foundation Trust, London, UKCorrespondence: Laura Turton, Hearing Link, 27–28, The Waterfront, Eastbourne, East Sussex, BN23 5UZ, UK. E-mail:[email protected]: To estimate the prevalence of severe and profound hearing loss in a clinical population and to report the audiological and hearing-aid characteristics for this group, as well as outcome measures from use of hearing aids. Design: A retrospective observational study initially, followed by a postal Glasgow health status inventory (GHSI) to establish the patients functional outcomes. Study sample: A clinical database of 32 781 cases was interrogated from which 2199 cases of severe /profound hearing loss were identified. From these, an adult sample stratified in terms of age and gender of n = 302 was contacted. Results: An estimated 6.7% of the local clinical population and 0.7% of the general population were found to have hearing > 70 dB averaged over 0.5, 1, and 2 kHz. Most patients were fitted with bilateral hearing aids, using a non-linear prescription, and as a group they reported a high level of social support. Conclusions: This study has estimated the prevalence of severe and profound hearing loss as 6.7% of the clinical population, and 0.7% of the general population. This is consistent with previous work, although it probably underestimates the prevalence. Further work is indicated to strengthen the estimate.
Symposium on hearing loss ‐ The otolaryngologist's responsibility.: Medical management of hearing loss.
AbstractMillions of Americans suffer hearing loss resulting in immense social and economic consequences. Hearing loss is merely a symptom or sign and the evaluation and management of afflicted individuals requires a thorough knowledge of etiologic factors and understanding of the underlying pathophysiology. Hearing loss is either conductive, sensorineural, or mixed. It may be congenital or delayed in onset, genetic or progressive or stable. Specific diagnosis should be sought in all cases with the objective being reversal of the hearing loss. Often definitive therapy is lacking yet prevention of progression, when possible; recognition of associated disorders, when present; compensation for disability, when applicable; epidemiologic study; genetic and psycho-social counseling; and habilitation and rehabilitation may still be initiated. A vigorous approach to the patient with hearing loss should be championed by the otolaryngologist.
Current Opinion in Neurology · 1999 · 11 citations
Vestibular and hearing loss in genetic and metabolic disorders
AbstractHearing loss affects about 4% of people under 45 years of age and comprises a broad spectrum of clinical presentations (congenital or late-onset, conductive or sensorineural, and syndromic or nonsyndromic). Approximately 30% of genetically determined deafness is reported to occur in syndromic form and 70% in nonsyndromic form. This review highlights recent advances in the molecular and genetic basis of hearing loss, which will help in understanding the biology of normal and abnormal hearing.
AbstractEpidemiological studies more than a century ago demonstrated that genetic factors are major contributors to hearing loss. Many genes associated with hearing loss have now been identified, although mutations in one of them, GJB2, explain a high proportion of genetic deafness in several populations. Environmental factors such as viruses (in particular, cytomegalovirus), ototoxic drugs, and noise also are associated with hearing loss, as is the aging process. Genetic hearing loss may be either syndromic (other organs and tissues are abnormal) or nonsyndromic. The majority show an autosomal recessive pattern of inheritance, but autosomal dominant, X-linked, and mitochondrial forms of hearing loss are found. In this article, four hearing loss syndromes, Jervell and Lange-Nielsen, Wolfram, branchio-otorenal, and Alport, are described; respectively, they are caused by mutations in genes encoding a potassium channel complex (KCNQ1, KCNE1), extracellular matrix proteins (COL4A3, COL4A4, COL4A5), transcription factors (EYA1, SIX1), and a protein that may be a novel endoplasmic reticulum calcium channel or a regulator of channel activity (WFS1). The contribution of mitochondrial DNA (mtDNA) mutations to hearing loss also is discussed.
Advanced Science · 2025 · 1 citations · open access
Hearing Loss: From Basic to Clinical Science
AbstractHearing loss (HL) affects over 1.5 billion people globally, with genetic factors accounting for ≈50% of congenital cases. Therefore, HL has become a global health issue, driving extensive research from basic science to clinical applications. This Special Collection includes a total of 31 papers, among which 9 are review papers, 21 are research article papers, 1 is a perspective paper, that highlight the basic mechanisms and possible protection methods of HL, the application of gene therapy for treating HL, and the clinical study and application in HL.
AbstractOur findings confirm the complex genetic landscape of hearing loss and the limitations of WES in achieving a 100% diagnostic rate, especially in conditions characterized by genetic heterogeneity. These results contribute to our understanding of the genetic basis of hearing loss and emphasize the need for further research and comprehensive genetic analyses to elucidate the underlying causes of this condition.
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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