DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for hearing loss, autosomal dominant 76 — 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 76 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 76 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
A 1995 study of one extended Dutch family with autosomal dominant progressive high-frequency hearing loss mapped the causative gene to a 15 cM interval on chromosome 7p15, between markers D7S493 and D7S632. That locus was designated DFNA5. No drug or treatment was tested. The abstract states that progressive hearing loss affects about 50% of people over 80 and is thought to involve both genetic and environmental factors, but offers no therapeutic intervention.
A 1978 symposium paper describes hearing loss as a symptom requiring a thorough search for cause, with the stated objective of reversal. It acknowledges that definitive therapy is often lacking, and that management may be limited to prevention of progression when possible, compensation for disability, and rehabilitation. No specific drug, gene, or trial is mentioned.
A 2020 study of cochlear implantation in children with DFNB7/11 (caused by TMC1 gene variants) included only three patients from two non-consanguineous families. All had prelingual severe-to-profound hearing loss. After implantation, speech perception, nonverbal cognition, and speech performance were reported as excellent and comparable to children with DFNB1 deafness. The authors note that their results do not support the variable auditory outcome reported elsewhere, and that social, environmental, and genetic factors may influence outcomes. No drug was tested.
A 2025 expert consensus on surgical treatment for hereditary hearing loss states that the condition is suitable for individualised precision medicine, but the document is a guidance plan for surgical methods, efficacy evaluation, and postoperative rehabilitation. No drug, no repurposing, and no pharmacological trial data are presented. What is missing for any drug-repurposing approach to DFNA5 hearing loss is a candidate drug, a molecular target, any preclinical or clinical efficacy data, and funding for a trial that would need to account for the genetic heterogeneity and phenotypic diversity noted in the consensus.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Human Molecular Genetics · 1995 · 103 citations
Localization of a gene for non-syndromic hearing loss (DFNA5) to chromosome 7p15
AbstractProgressive hearing loss affects approximately 50% of the elderly by the age of 80, and is most likely caused by an interaction of genetic and environmental factors. Identification of the genes responsible for hereditary hearing loss is therefore important. Families with pure genetic degenerative hearing disorders may be helpful as the same genes may be also involved in age-related hearing loss in general. In this study we have performed a genome search in an extended Dutch family with autosomal dominant progressive hearing loss starting in the high frequencies. The gene causing hearing loss in this family was localized to the short arm of chromosome 7, in a 15 cM interval between markers D7S493 and D7S632.
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.
Amrita Journal of Medicine · 2020 · 9 citations · open access
Hearing loss: A neglected and morbid clinical entity in Corona Virus Disease 2019 pandemic
AbstractHearing loss may be caused by certain viral infections. The hearing loss due to viral infection can be congenital or acquired, bilateral or unilateral. The viral infections typically cause sensorineural hearing loss (SNHL), although conductive or mixed hearing loss can be found. The corona virus disease 2019 (COVID-19) infection has deleterious impact on the cochlear hair cells. The hearing loss will not improve even patient recovered from COVID-19 infections. This is probably a neuro-auditory involvement in COVID-19 infections. The current COVID-19 is caused by severe acute respiratory syndrome corona virus 2. The audiologic and radiologic investigations are helpful for evaluation of the hearing loss in COVID-19 patients. Hearing loss due to COVID-19 infections is rarely reported in medical literature so far. Hearing loss specifically SNHL is often challenging to the clinicians in this current pandemic. The mechanism for this deleterious effect on the cochlear hair cells requires further research. There is a large gap in the understanding of the etiopathogenesis, epidemiology, and clinical presentations such as hearing loss and human transmission of this disease. There should be a continuous monitoring of the hearing loss and tracing of this COVID-19 infection is needed to ensure the detail understanding of this inner ear pathogenesis. This review article provides an overview of COVID-19 infections and its impact on hearing loss.
American Journal of Medical Genetics Part A · 2023 · 2 citations · open access
Cause, severity, and efficacy of treatment for hearing loss in children with Trisomy 18: A single institution‐based retrospective study
AbstractTrisomy 18 is a common chromosomal aberration syndrome, characterized by variable clinical manifestations, including cardiovascular, pulmonary, genitourinary, and musculoskeletal findings, leading to a shorter survival and severe developmental delay in survivors. However, recently, intensive therapeutic intervention has allowed for prolonging survival. In terms of otological complications, only a limited number of relevant reports have been published. To demonstrate the characteristic of hearing loss (HL) in children with Trisomy 18, we retrospectively evaluated 22 patients (44 ears) by comprehensive auditory evaluation with the auditory steady-state response (ASSR) test and temporal bone computed tomography (CT). ASSR revealed that 20 patients (91%) had bilateral moderate to profound HL, more frequent and severe than that in Trisomy 21; among 42 ears having HL, 12 ears (29%) had conductive HL, and 26 ears (62%) had mixed HL. CT scans of 38 ears revealed that 34 ears (89%) had an external and middle ear malformation. Hearing aids (HA) were fitted in 17 patients (air and bone-conduction HAs). The threshold hearing with HA was improved in all of them. Accurate otological evaluation using ASSR and CT and intervention by HAs could be a feasible choice for children with Trisomy 18.
Supplementary Material for: Auditory Outcome after Cochlear Implantation in Children with DFNB7/11 Caused by Pathogenic Variants in <b><i>TMC1</i></b> Gene
Abstract<b><i>Introduction:</i></b> Non-syndromic hereditary hearing loss is characterized by extreme genetic heterogeneity. So far, more than 100 pathogenic or likely pathogenic variants in <i>TMC1</i> gene have been reported in patients with autosomal recessive hearing loss (HL) DFNB7/11. The prevailing auditory phenotype of individuals with DFNB7/11 is congenital, profound, bilateral HL, but the functional outcome after cochlear implantation (CI) described in the literature is variable. The objective of this work is to evaluate the auditory outcome after CI in pediatric patients with DFNB7/11, born to non-consanguineous parents. <b><i>Methods:</i></b> A retrospective analysis of genetic and audiological data of DFNB7/11 patients followed up in a single Italian otolaryngology clinic was performed. Cases with biallelic pathogenic variants in <i>TMC1</i> were selected from the cohort of children with non-syndromic hearing loss who had undergone CI and had been molecularly characterized by multigene panel testing. All patients underwent extensive audiological assessment, and the auditory outcome after CI was evaluated. <b><i>Results:</i></b> DFNB7/11 was diagnosed in a total of 3 patients from 2 non-consanguineous families; a novel disease-causing variant in <i>TMC1</i> was detected [c.962G>A p.(Trp321*)]. All the affected children showed the typical DFNB7/11 phenotype characterized by prelingual, severe-to-profound HL. The patients showed an excellent functional outcome after CI; speech perception, nonverbal cognition, and speech performance were comparable to those of patients with DFNB1 deafness. <b><i>Discussion/Conclusion:</i></b> Our results do not support the variable auditory outcome reported in the literature, which may be affected by several social and environmental factors and by the genetic background.
[Expert consensus on surgical treatment for hereditary hearing loss].
AbstractHereditary hearing loss, with its well-defined molecular etiology, is a typical disease suitable for applying the concept of individualized precision medicine to clinical practice. Given its genetic heterogeneity and phenotypic diversity, there are particularities for the surgical treatment of hereditary hearing loss. Based on the results of the molecular epidemiological survey of large samples of deafness, various surgical methods and postoperative follow-up data, this expert consensus formulates a detailed guidance plan for the surgical treatment, efficacy evaluation and postoperative rehabilitation of hereditary hearing loss.
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.
