DeCure for Autosomal dominant nonsyndromic hearing loss 70
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for autosomal dominant nonsyndromic hearing loss 70 — 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 moduleAutosomal dominant nonsyndromic hearing loss 70 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 autosomal dominant nonsyndromic hearing loss 70 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
The abstracts cover autosomal dominant nonsyndromic hearing loss, but none of them describe a drug or treatment for the condition itself. One 1995 study localised a gene for autosomal dominant progressive hearing loss (DFNA5) to chromosome 7p15 in a single extended Dutch family, using a 15 cM interval between markers D7S493 and D7S632. A 1993 paper describes two kindreds with autosomal dominant progressive sensorineural hearing loss beginning in the early 20s, affecting high frequencies first, with almost complete penetrance across four generations; 23 of 74 members were affected. A 2000 review notes that monogenic forms of hearing loss can be syndromic or nonsyndromic, but provides no treatment data.
The only intervention discussed is cochlear implantation, and only for a recessive form (DFNB7/11) caused by TMC1 variants, not for autosomal dominant hearing loss 70. In three children from two non-consanguineous families with DFNB7/11, all had prelingual severe-to-profound hearing loss and showed excellent functional outcome after cochlear implantation, with speech perception and performance comparable to DFNB1 deafness patients. The authors state their results do not support the variable auditory outcome reported elsewhere.
No drug, no molecular therapy, no clinical trial for autosomal dominant nonsyndromic hearing loss 70 appears in these abstracts. What is missing is any drug candidate, any preclinical or clinical trial funding, any patient stratification by specific DFNA5 or other dominant gene variant, and any trial design that could test a pharmacological intervention for this specific form of hearing loss.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
New England Journal of Medicine · 2000 · 202 citations
Genetic Causes of Hearing Loss
AbstractHearing loss is the most common sensory defect in humans, affecting normal communication in 10 percent of people aged 65 years or older. In most cases, hearing loss is a multifactorial disorder caused by both genetic and environmental factors. However, single-gene mutations can lead to hearing loss. In these cases, hearing loss is a monogenic disorder with an autosomal dominant, autosomal recessive, X-linked, or mitochondrial mode of inheritance. These monogenic forms of hearing loss can be syndromic (characterized by hearing loss in combination with other abnormalities) or nonsyndromic (with only hearing loss). This review focuses on nonsyndromic hearing loss, since . . .
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.
Archives of Otolaryngology - Head and Neck Surgery · 1993 · 51 citations
Autosomal Dominant Sensorineural Hearing Loss: Further Temporal Bone Findings
AbstractIn a previous publication, my colleagues and I<sup>1</sup>described the audiologic and temporal bone characteristics of some affected members in two kindreds with autosomal dominant progressive sensorineural hearing loss.<sup>1</sup>The pedigree and audiologic and temporal bone findings of kindred 1 are briefly summarized here, and additional temporal bone findings are described. <h3>PREVIOUS FINDINGS</h3> Kindred 1 consists of 74 members from four generations. The hearing status of 26 members is unknown. Of the 23 affected members, 12 are male and 11 are female. The pattern of trait inheritance is autosomal dominant, with almost complete penetrance. By history and analysis of available audiograms of affected and unaffected individuals, we determined that the hearing loss begins in the early 20s. None of the fourth-generation members have attained the age of 20 years and, presumably for this reason, have normal hearing. The hearing loss is progressive, high frequencies being affected first, followed
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.
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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