DeCure's autonomous Psychiatry AI scientist is researching a drug-repurposing hypothesis for intellectual developmental disorder 61 — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleIntellectual developmental disorder 61 maps to a 3-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 developmental disorder 61 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
WD repeat domain 1 (WDR1) — WDR1 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 adpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9QFQ · 2.76 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
Intellectual developmental disorder, comprising global developmental delay and intellectual disability, affects 1% to 3% of children, with a global prevalence estimated at 6% to 8%. It is defined by limitations in intellectual functioning (IQ below 70) and adaptive behaviour starting before 18 years of age. The condition carries substantial comorbidity, high lifetime costs, and emotional burden. Two-thirds of cases have an unknown aetiology. The causes are heterogeneous, ranging from environmental factors to chromosomal and monogenic conditions. Balanced chromosomal translocations, found as de novo events in 1 in 2,000 live births, can produce abnormal phenotypes through submicroscopic deletions, duplications, inversions, or disruption of genes at breakpoints, though cryptic genomic imbalances causing intellectual disability are very rare.
No pharmacological intervention has been shown to alter the underlying cognitive deficits in intellectual developmental disorder. Current medical practices aim only at relieving symptoms. Scientific advances have raised the possibility that intellectual disability might become treatable, with fragile X syndrome proposed as a benchmark for central nervous system drug discovery, but no such therapy is established. One review claimed that homeopathic medicine will remove the disease from the root cause, but provided no data, no sample sizes, no response rates, and no survival figures to support that claim. The limited availability of mouse models of intellectual disability further hampers preclinical research.
Molecular genetics has advanced with next-generation sequencing, identifying that multiple copy number variations can lead to intellectual disability or developmental delay. Pinpointing a precise genetic cause allows accurate genetic counselling, avoidance of unnecessary testing, prognostication, and tailored management for an increasing number of conditions. Still, only a small number of autosomal genes responsible for intellectual disability have been identified, with most progress made in X-linked translocation forms. The complex molecular basis remains largely unknown.
What is still missing is adequate funding for large-scale genomic studies to resolve the two-thirds of cases with unknown cause, properly designed clinical trials for any candidate therapy, and better patient stratification by genetic subtype so that targeted interventions can be tested in homogeneous populations rather than the heterogeneous group currently labelled intellectual developmental disorder.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
CONTINUUM Lifelong Learning in Neurology · 2018 · 21 citations · open access
Evaluation of the Child With Developmental Impairments
AbstractPURPOSE OF REVIEW: This article discusses the diagnostic evaluation of intellectual developmental disorder, comprising global developmental delay and intellectual disability in children. RECENT FINDINGS: With a prevalence of 1% to 3% and substantial comorbidity, high lifetime costs, and emotional burden, intellectual developmental disorder is characterized by limitations in both intellectual functioning (IQ less than 70) and adaptive behavior starting before 18 years of age. Pinpointing the precise genetic cause is important, as it allows for accurate genetic counseling, avoidance of unnecessary testing, prognostication, and tailored management, which, for an increasing number of genetic conditions, targets the pathophysiology and improves outcomes. SUMMARY: The etiology of intellectual developmental disorder is heterogeneous, which mandates a structured approach that considers family situation, test costs, yield, and potential therapeutic tractability of the identified condition. Diagnosis of an underlying genetic cause is increasingly important with the advent of new treatments. Still, in many cases, the cause remains unknown, and research is needed to elucidate its complex molecular basis.
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.
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.
International journal of pediatrics · 2018 · 0 citations
Advances in molecular genetics of intelligence disability or developmental delay
AbstractIntelligence disorder or developmental delay is the defect of cognitive function and social adaptation function as the main clinical features, two-thirds of the etiology is unknown.Clinical manifestations, high morbidity, and low treatment outcome are the major challenge for us.In recent years, with the application of the new generation of sequencing technology, We have gained further understanding of the etiology and pathogenesis of intelligent disorder or developmental delay.It has been found that multiple copies of chromosomal copies can lead to it.This paper summarizes the clinical, imaging and etiology of intelligent disorder or developmental delay, especially the recent advances in molecular genetics.
Key words:
Developmental delay; Etiology; Mutation
DOAJ (DOAJ: Directory of Open Access Journals) · 2023 · 0 citations · open access
How might a balanced chromosomal translocation lead to a spectrum of intellectual disabilities in newborns?
AbstractBackground: Intellectual disability (ID) consists of a broad range of disorders characterized by low general intellectual functioning (IQ below 70). ID etiologic causes are heterogeneous, ranging from environmental to chromosomal and monogenic conditions. Although many autosomal genes responsible for ID are expected, but only a small number of these have been identified and up to now most progress has been made in the area of X-linked translocation ID; but many autosomal chromosome genes play a crucial role in the development of a central nervous system. Any change which lead to lose or reduce the function or change the expression of them; high or low, even have a damaging effect on the functional protein might lead to different phenotype like developmental delay, growth retardation or intellectual disabilities. Result & conclusion: In this paper, we discuss the importance of balanced chromosomal translocations in the etiologic cause of newborn intellectual disabilities. Balanced translocation is the result of breaking off two chromosomes and reattached in a way that the sections of two chromosomes have switched places. These rearrangements are found as de novo events in 1/2,000 live births and give rise to some congenital anomalies which is the product of submicroscopic deletions, duplications, inversion or disruption, activation, or inactivation of a gene or different genes located at or near the breakpoints in the basepair level. These apparently balanced translocations due to positional effect lead to occur abnormal phenotype. In conclusion, Cryptic genomic imbalances cause mentality are very rare condition but new technologies like NGS long-read genome sequencing could detect rapid breakpoint effects on live birth healthy and discover a new way for prenatal diagnosis.
Journal of Pediatric Nephrology · 2015 · 0 citations · open access
Williams-Beuren Syndrome: Manifestation with Attention Deficit Hyper Activity Disorder and Voiding Dysfunction with Kidney Anomalies; Good Response to Ritalin
AbstractWilliams-Beuren syndrome is a rare neurodevelopmental disease, in which mental retardation is common with this submicroscopic chromosomal deletion genetically disease. We reported a boy with Williams-Beuren syndrome and highlighted the clinical characteristics and response to treatment with Ritaline of such an individual with ADHD and voiding dysfunction. The patient was a six year-old boy with typical presentation of WBS and some psychiatric problems referred because of hyperactivity symptom and attention deficit. Children with mental retardation and WBS have a comorbidity of psychiatric disorders and kidney anomalies. Williams-Beuren syndrome can present with hyperactivity and Ritalin can improve some symptoms and voiding dysfunction. Keywords: Williams-Beuren Syndrome; Attention Deficit Disorder with Hyperactivity; Ritalin ; Methylphenidate.
Growth and development four years after treatment for the Trichuris dysentery syndrome
AbstractA follow-up study is reported of 18 children 4 y after treatment for the Trichuris dysentery syndrome (TDS) and matched control children. The TDS children were initially severely stunted and had extremely low developmental levels. They showed catch-up in height of 1.9 z-scores even though they remained in very poor environments. Their intelligence quotients, school achievement and cognitive function remained significantly lower than those of the controls. Controlling for their earlier developmental levels, the TDS children showed a small improvement in mental development relative to the controls.
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.
