DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for Meesmann corneal dystrophy — 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 moduleMeesmann corneal dystrophy 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 meesmann corneal dystrophy 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
Meesmann corneal dystrophy is a non-progressive autosomal dominant epithelial dystrophy characterised by intraepithelial cysts, likely caused by an intraepithelial metabolic abnormality. In a postmortem study of an 84-year-old patient who had a penetrating keratoplasty in one eye and a lamellar keratoplasty in the other, the characteristic features of Meesmann dystrophy recurred in the donor cornea of the grafted eye. The findings were limited to the epithelium and included increased thickness, architectural disorganisation, loss of cell polarity, increased intracellular glycogen, intraepithelial microcysts containing degenerated cells, and an electron-dense fibrillogranular material associated with disrupted cytoplasmic filaments. The authors concluded that the abnormalities causing the disease are localised to the corneal epithelial cells, not the stroma.
Cases may be asymptomatic or cause irritation, lacrimation, and photophobia. Palliative treatment includes ocular lubricants, cycloplegia, and therapeutic contact lenses. In severe cases, epithelial debridement, phototherapeutic keratectomy, and lamellar keratoplasty have been advocated. A 2009 report described a case with unusually severe symptoms and punctate epithelial keratopathy managed with a therapeutic contact lens. A 2008 case report noted a rare occurrence of Meesmann dystrophy concurrent with epithelial basement membrane dystrophy and posterior polymorphous corneal dystrophy in a 6-year-old boy observed for 24 years. Confocal microscopy has been used to image the corneal microstructure in these dystrophies, with both slit-scanning and laser-scanning devices providing diagnostically helpful images.
No controlled trials of any drug therapy for Meesmann corneal dystrophy were reported in these abstracts. The genetic basis involves mutations in genes encoding corneal epithelial keratins, but no targeted molecular treatment has been tested. What remains missing is any clinical trial of a pharmacological intervention, a clear understanding of which patients progress to severe symptoms, and a stratified approach to selecting between debridement, phototherapeutic keratectomy, or keratoplasty based on long-term outcomes.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Cornea · 1998 · 21 citations
Recurrent Meesmannʼs Corneal Epithelial Dystrophy After Penetrating Keratoplasty
AbstractPURPOSE: To characterize the histopathology of recurrent Meesmann's corneal epithelial dystrophy after penetrating keratoplasty. METHODS: Postmortem examination by light and electron microscopy of the eyes of an 84-year-old patient with Meesmann's dystrophy who underwent a penetrating keratoplasty in the right eye at age 74 years and a lamellar keratoplasty in the left eye at age 51 years. RESULTS: In the right eye, the characteristic features of Meesmann's dystrophy were demonstrated in both the donor and recipient corneas. The pathologic findings were limited to the corneal epithelium and included increased thickness, architectural disorganization, loss of cell polarity, increased amounts of intracellular glycogen, presence of intraepithelial microcysts containing degenerated cells, and in some cells, the presence of an electron-dense fibrillogranular material associated with disrupted cytoplasmic filaments. In the left eye, the corneal findings were consistent with but not specific for Meesmann's dystrophy. These included architectural disorganization, loss of cell polarity, presence of intraepithelial microcysts, and irregular thickening of the basement membrane in the donor cornea. CONCLUSION: Meesmann's corneal epithelial dystrophy is demonstrated to recur after penetrating keratoplasty. This finding suggests that the abnormalities that lead to the disease are localized to the corneal epithelial cells and not in the stroma, as previously proposed.
Optometry and Vision Science · 2009 · 11 citations
Management of Symptomatic Meesmann Dystrophy
AbstractMeesmann dystrophy is a non-progressive autosomal dominant corneal epithelial dystrophy characterized by intraepithelial cysts, which is likely to be caused by an intraepithelial metabolic abnormality. Cases may be asymptomatic or be associated with symptoms of irritation, lacrimation, and photophobia. Palliative treatment includes ocular lubricants, cycloplegia, and therapeutic contact lenses. In severe cases, management with epithelial debridement, phototherapeutic keratectomy, and lamellar keratoplasty has been advocated. Most recently, the genetic and molecular basis of Meesmann dystrophy have been explored, and mutations in the genes encoding corneal epithelial keratins have been reported. This report describes a case of Meesmann dystrophy with unusually severe symptoms and punctate epithelial keratopathy managed with a therapeutic contact lens.
Klinische Monatsblätter für Augenheilkunde · 2006 · 10 citations
Konfokale Scanning-Mikroskopie: Eine vergleichende Darstellung von Hornhautdystrophiebefunden mittels ConfoScanP2 und Rostock Cornea Modul-HRT II
AbstractBACKGROUND: The object of this work was a comparison of confocal images of corneal dystrophies made by a slit scanning microscope versus a laser scanning microscope. MATERIAL AND METHODS: Using the Rostock Cornea Modul-HRT II as a confocal laser scanning microscope the images of five patients with some epithelial, stromal and endothelial corneal dystrophies were acquired. The pictures were compared qualitatively with those taken by the slit scanning microscope "ConfoScan P2" from corresponding pathologies. Also, the images of normal corneas of ten healthy persons were acquired for a qualitative comparison. RESULTS: Confocal images from both devices were able to provide significant helpful diagnostic findings about the corneal microstructure. Essential qualitative differences between the images of both devices used were not observed. Due to the additional hardware components and the software module for image acquisition, analysis and archiving, the RCM-HRT II is favoured over the "ConfoScan P2". Nevertheless, the evaluation in favour of the RCM-HRT II has to be confined because an optimised, user-friendly enhancement, the "ConfoScan 4" is currently available. CONCLUSION: Evaluating corneal dystrophies in vivo, an equivalent utility of both technical approaches has been observed.
Meesmann Corneal Dystrophy Associated With Epithelial Basement Membrane and Posterior Polymorphous Corneal Dystrophies
AbstractPURPOSE: To report a rare case of bilateral and symmetric Meesmann corneal dystrophy concurrent with bilateral epithelial basement membrane dystrophy and bilateral but asymmetric posterior polymorphous corneal dystrophy in a patient of Armenian origin. METHODS: Complete ophthalmologic examination was performed on a 6-year-old boy from Armenia who was diagnosed with bilateral symmetric Meesmann corneal dystrophy combined with bilateral epithelial basement membrane dystrophy and bilateral but asymmetric posterior polymorphous corneal dystrophy. This case was observed and treated for 24 years. RESULTS: On slit-lamp biomicroscopy, the patient showed bilateral multiple intraepithelial cystic lesions, bilateral irregularly shaped grayish-white opacities in the superficial corneal epithelium, and bilateral but asymmetric transparent vesicles surrounded by gray halos at the level of the Descemet membrane and the endothelium. CONCLUSIONS: This case is reported because of the unusual occurrence of Meesmann corneal dystrophy with other corneal dystrophies.
Journal of the Foundations of Ophthalmology · 2023 · 0 citations
An Overview of Epithelial and Stromal Corneal Dystrophies
AbstractPrincipally, corneal dystrophies are a set of conditions that impact corneal transparency and distorts corneal structure. They are commonly bilateral, progressive, and differs from corneal degeneration as they are often inherited through autosomal dominant or recessive modes as well as x-linked modes. Several genes have been implicated in corneal dystrophies and will be elaborated on in the description of dystrophies in this article. Management of corneal dystrophies depend on severity of symptoms and require specialist input. Mildly symptomatic dystrophies do not warrant management. However, in those with progressive disease and/or poor vision, surgical options may be of use. Techniques commonly involved in the management of dystrophies include deep lamellar endothelial keratoplasty, penetrating keratoplasty, or the area of disease is ablated using a photo-therapeutic keratectomy.
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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