DeCure for Intellectual disability, autosomal dominant 57
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for intellectual disability, autosomal dominant 57 — 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 moduleIntellectual disability, autosomal dominant 57 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 intellectual disability, autosomal dominant 57 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.
Molecular view
tousled like kinase 2 (TLK2) — TLK2 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet agsdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 5O0Y · 2.86 Å · ligand PHOSPHOTHIOPHOSPHORIC ACID-ADENYLATE ESTER (AGS). Experimental structure, not a prediction.
What the evidence adds up to
The three abstracts provided do not contain any clinical trial data, survival statistics, response rates, or sample sizes for any drug in intellectual disability, autosomal dominant 57. The 2011 update on Fragile X syndrome states that intellectual disability was considered immutable and that current practice aims at symptom relief, not altering cognitive deficits. It mentions the possibility that pharmaceutical therapies targeting Fragile X syndrome might become a benchmark for CNS drug discovery, but gives no concrete results. The 2008 text describes a diagnostic manual for mental disorders in people with intellectual disability and provides no treatment data. The 2022 paper on Bardet-Biedl syndrome mouse models notes that intellectual disability affects 1% of the global population, is characterised by deficits in intellectual and adaptive functioning, and that pharmacological interventions are limited due to poor understanding and heterogeneity. It adds that there are limited mouse models of intellectual disability.
No abstract mentions autosomal dominant 57 specifically. No drug, no response rate, no survival figure, no sample size appears in any of the three texts. The 2011 abstract offers a hopeful statement about treatability but provides no evidence. The 2022 abstract explicitly states that pharmacological interventions are limited.
What is missing for intellectual disability, autosomal dominant 57 is any clinical or preclinical study of a drug in that specific genetic subtype. The abstracts highlight a general lack of mouse models and a poor understanding of the heterogeneous causes of intellectual disability. Without a dedicated trial, a validated animal model, or a stratified patient cohort, no conclusion about any treatment for this condition can be drawn.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
ACS Chemical Neuroscience · 2011 · 19 citations · open access
Fragile X Syndrome: An Update on Developing Treatment Modalities
AbstractIntellectual disability (ID; mental retardation) is considered an immutable condition. Current medical practices are aimed at relieving symptoms and not at altering the underlying cognitive deficits. Scientific advancements from the past decade have led to the exciting possibility that ID may now be treatable. Moreover, pharmaceutical therapies targeting the most common form of inherited ID, Fragile X syndrome (FXS), may become the new benchmark for central nervous system (CNS) drug discovery: seeking cures for neurodevelopmental disorders.
Mental Illness and Intellectual DisabilityMental Illness and Intellectual Disability
AbstractThe Diagnostic Manual—Intellectual Disability: A Textbook of Diagnosis of Mental Disorders in Persons with Intellectual Disability (DM–ID) provides adaptations of the diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM–IV–TR; American Psychiatric Association, 2000) that will facilitate more accurate diagnosis of psychiatric conditions in people with intellectual disability (ID). The text also provides a review of the relevant scientific literature for each condition and a rating of the strength of the evidence supporting assertions in the literature. The volume is the product of considerable effort; the four editors were assisted in their task by a 10member advisory board, seven external peer reviewers, dozens of Diagnostic Manual—Intellectual Disability: A
Biopolymers and Cell · 2015 · 1 citations · open access
Association of the EPHA1 gene polymorphism with idiopathic mild intellectual disability
AbstractTo investigate a possible association of the EPHA1 gene polymorphism with mild intellectual disability (ID). Methods. The group of patients with mild (IQ score between 50 and 70) idiopathic intellectual disability consisted of 65 individuals including 41 (63.1 %) males and 24 (36.9 %) females. The control group consisted of 250 healthy volunteers from different regions of Ukraine. The genotyping was performed using PCR followed by RFLP analysis for rs11768549, rs11767557, rs11771145 and ARMS PCR analysis for novel c.1891G>A EPHA1 gene mutation. Results. The data concerning the EPHA1 genotypes and allelic variants distribution in ID patients and control group were obtained. Statistical analysis showed a signifi cant association of minor rs11768549-A allele (OR = 3.96, 95 % CI = 1.13-13.89) and wild-type rs11767557-T (OR = 1.99, 95 % CI = 1.18-3.37) and rs11771145-G (OR= 1.55, 95 % CI = 1.02-2.37) alleles with a higher risk of mild ID development (p < 0.05 for all). Conclusions. Our results suggest that SNPs (rs11768549, rs11767557, rs11771145) in the EPHA1 gene are associated with idiopathic mild intellectual disability. Therefore, we propose the EPHA1gene as a new candidate gene and the polymorphisms rs11768549, rs11767557, rs11771145 as new markers of genetic susceptibility for intellectual disability.
Iowa Research Online (The University of Iowa) · 2022 · 0 citations · open access
Behavioral and brain phenotypes of mouse models of Bardet-Biedl Syndrome
AbstractIntellectual disability (ID) is one of the most common neurodevelopmental disorders, affecting 1% of the population globally. Clinically, ID is characterized by a deficit in intellectual functioning and adaptive functioning. There are limited pharmacological interventions for ID, partially due to a poor understanding of ID and the heterogeneous nature of ID In addition, there are limited mouse models of ID.
International Journal of Homoeopathic Sciences · 2022 · 0 citations · open access
An overall review on intellectual disability disorder and its homoeopathic management
AbstractThe Intellectual Disability Disorder is found as a one of the clinical manifestations of the rare disorders which occupies a total prevalence of about 6 to 8% globally. The rare disorder is found to cause many of the chronic disabilities in which the intellectual disability disorder is one of them which has a drastic impact on the individual who is affected and their families and includes the health care system. The onset period of the rare disorder begins from the prenatal period into the late adulthood and it is being assessed that about the half of the individual affected are children [1]. The prime and the only purpose of this study undertaken is to find the effectiveness of the homoeopathic medicine in the treatment of the Intellectual Disability Disorder and also to alter their intellectual and the adaptive functions of the affected individual. The homoeopathic medicine will remove the disease from the root cause.
AbstractMapping of the 6q16.1 deletions encompassing EPHA7 (highlighted in blue) in our patients (red bar). Four out of 12 patients have deletions encompassing only EPHA7 and share a similar phenotype, suggesting the role of EPHA7 deletion as a risk factor for neurodevelopmental disorder with developmental delay/intellectual disability, speech delay, behavioral anomalies, and/or microcephaly. The deletions were inherited in nine out of 12 patients, suggesting variable expressivity and incomplete penetrance.
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.
