DeCure for Autosomal recessive spinocerebellar ataxia 18
DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for autosomal recessive spinocerebellar ataxia 18 — 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 recessive spinocerebellar ataxia 18 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 recessive spinocerebellar ataxia 18 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
glutamate ionotropic receptor delta type subunit 2 (GRID2) — GRID2 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 apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 9NWO · 3.57 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
The abstracts provided do not contain any data on autosomal recessive spinocerebellar ataxia 18, nor do they report any drug trials, treatment outcomes, or interventional studies. One 2005 review summarises the genetic and clinical heterogeneity of hereditary ataxias, noting that the expanding number of genes and loci complicates patient management, but gives no specific figures for any subtype. A 2025 case report describes a 34-year-old patient with spinocerebellar ataxia type I, an autosomal dominant form, and observes that clinical symptoms appeared before neuroimaging changes; it contains no therapeutic information. A 2000 chapter on familial adult-onset spinocerebellar degenerations estimates prevalence between 1.5 and 22.1 per 100,000 and discusses classification difficulties, again without mentioning any drug or treatment.
No evidence of efficacy for any compound in autosomal recessive spinocerebellar ataxia 18 can be extracted from these texts. There are no response rates, survival statistics, or sample sizes relevant to this disease. The only concrete clinical observation is the single case of dominant ataxia type I, which is a different condition and offers no basis for drug repurposing. The abstracts are reviews and a case report, not clinical trials, so no conclusions about pharmacological intervention are possible.
What is missing is any primary research on autosomal recessive spinocerebellar ataxia 18 itself, including natural history data, biomarker studies, or preclinical models that could identify a druggable target. No funding for such work is mentioned, and no trial design or patient stratification strategy is proposed in these documents. Without that foundational evidence, no drug can be assessed for this specific ataxia.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Recent Advances in Hereditary Spinocerebellar Ataxias
AbstractIn recent years, molecular genetic research has unraveled a major part of the genetic background of autosomal dominant and recessive spinocerebellar ataxias. These advances have also allowed insight in (some of) the pathophysiologic pathways assumed to be involved in these diseases. For the clinician, the expanding number of genes and genetic loci in these diseases and the enormous clinical heterogeneity of specific ataxia subtypes complicate management of ataxia patients. In this review, the clinical and neuropathologic features of the recently identified spinocerebellar ataxias are described, and the various molecular mechanisms that have been demonstrated to be involved in these disorders are discussed.
South Russian Journal of Therapeutic Practice · 2025 · 1 citations · open access
A familial case of spinocerebellar attack type I. Clinical and diagnostic parallels
AbstractSpinocerebellar ataxia is a neurodegenerative disease with an autosomal dominant type of inheritance, rapid progression of clinical manifestations with onset at a young age. The clinical case of a 34-year-old patient with spinocerebellar ataxia type I, burdened by a hereditary history and the formation of the anticipation phenomenon, is considered. It was noted thatclinical symptoms preceded neuroimaging data.
AbstractThe familial spinocerebellar degenerations are a heterogeneous group of disorders with onset in both childhood and adulthood. Their prevalence is estimated to be between 1.5 and 22.1 per 100,000. Although pathologic and clinical classification systems have been proposed in the past, all have had shortcomings. In the past several years, great strides in genetics have radically changed our thinking about the classification, and thus clinical presentation, of these disorders. In this chapter, we concentrate on the adult-onset familial ataxias.
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.
