DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for basal ganglia disease — 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 moduleBasal ganglia disease 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 basal ganglia disease 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
interferon induced with helicase C domain 1 (IFIH1) — IFIH1 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 9LOV · 3.07 Å · ligand ADENOSINE-5'-DIPHOSPHATE (ADP). Experimental structure, not a prediction.
What the evidence adds up to
The 2011 review of the basal ganglia model notes that the current pathophysiological framework was introduced two decades earlier and has shaped understanding of both normal and diseased basal ganglia function. The authors state that several questions remain unresolved and identify major challenges that need to be addressed, but provide no patient data, no treatment outcomes, and no specific disease-modifying interventions.
A 2003 case report describes foreign accent syndrome following a right basal ganglia injury. The authors note that fewer than twenty specific studies of this speech disorder existed at the time, and they discuss the possible role of the basal ganglia in its emergence. No treatment or outcome data are reported.
A 2008 case report describes biotin-responsive basal ganglia disease, a rare entity with ten previously reported cases. The authors present a new case that presented earlier, was milder, and responded better to lower doses of biotin than earlier cases. They note that this case might represent a new entity or a milder form of the same condition. The report is limited to a single patient.
A 1942 book on diseases of the basal ganglia is listed but no abstract is provided, so no clinical data can be extracted from it.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Frontiers in Neuroanatomy · 2011 · 67 citations · open access
Past, Present, and Future of the Pathophysiological Model of the Basal Ganglia
AbstractThe current model of basal ganglia (BG) was introduced two decades ago and has settled most of our current understanding of BG function and dysfunction. Extensive research efforts have been carried out in recent years leading to further refinement and understanding of the normal and diseased BG. Several questions, however, are yet to be resolved. This short review provides a synopsis of the evolution of thought regarding the pathophysiological model of the BG and summarizes the main recent findings and additions to this field of research. We have also tried to identify major challenges that need to be addressed and resolved in the near future. Detailed accounts and state-of-the-art developments concerning research on the BG are provided in the articles that make up this Special Issue.
Una rara alteración del habla de origen neurológico: El Síndrome del Acento Extranjero
AbstractINTRODUCTION: Foreign accent syndrome (FAS) is an unusual neurological speech disorder documented in not more than twenty specific studies. As a consequence of a cerebral mainly subcortical injury, the patient s speech is foreign sounding to native listeners. As subject cannot avoid this foreign accent, and given its abrupt emergence, this disorder usually involves emotional consequences by loss of identity and of belonging to a speech community. CASE REPORT: In this paper, a case from Castellón de la Plana (Spain) is presented with a injury in right basal ganglia and the literature about this topic is revised. CONCLUSIONS: From the available data, we describe the main characteristics of the syndrome and discuss the possible role of basal ganglia
Biotin-Responsive Basal Ganglia Disease: Case Report and Review of the Literature
AbstractBiotin-responsive basal ganglia disease is a rare entity of which 10 cases have been reported in the literature. We report a case of biotin-responsive basal ganglia disease with similarities and differences compared to the previously reported cases by Ozand et al. Our case presented much earlier, was milder and responded better to lower doses of biotin, compared to the cases reported previously. Since our case showed differences with those in the literature, it might represent a new entity or a milder form of the same entity.
AbstractJournal Article Diseases of the Basal Ganglia Get access Diseases of the Basal Ganglia. Edited by Tracy J. Putnam, M. D., (Chairman), Angus M. Franz, M. D., and S. Walter Ranson, M. D. Cloth. Price, $10. Pp. 719, with 268 illustrations. Baltimore: The Williams and Wilkins Company, 1942. Physical Therapy, Volume 22, Issue 3, May 1942, Page 172, https://doi.org/10.1093/ptj/22.3.172b Published: 01 May 1942
AbstractAbstract Parkinson's disease is the most common basal ganglia disorder that is caused by the degeneration of dopaminergic neurons in the substantia nigra. This article reviews the normal physiology of the basal ganglia in the normal state, as well as the pathophysiology of Parkinson's disease (PD) and other movement disorders associated with the basal ganglia. Also discussed is the pathophysiological basis for the surgical treatment of PD.
Correlation of response to subthalamic deep brain stimulation in Parkinson’s disease patients with striatal dopamine transporter density on 99mtc-TRODAT-1 SPECT
AbstractBACKGROUND: Deep brain stimulation (DBS) is a surgical approach with electrical stimulation of certain parts of the brain, which reduce Parkinson's disease (PD) symptoms. Since the loss of dopaminergic neurons in the substantia nigra is the main pathophysiology of PD, we aimed to evaluate the association of response to DBS with preoperative dopamine transporter density (DAT) and its postoperative changes in PD patients who underwent the bilateral implantation of the electrodes in the subthalamic nucleus (STN). METHOD: A prospective evaluation of Parkinson's disease patients who underwent STN-DBS for 2 years was done. 99mTc-TRODAT-1 single-photon emission computed tomography (SPECT) scan and assessment of PD using unified Parkinson's disease rating scale (UPDRS) III were performed in both pre- and post-operation states. The correlation of response to DBS after 6 months was assessed with baseline findings and postoperative changes of 99mTc-TRODAT-1 SPECT parameters. RESULTS: Compared to the preoperative state, UPDRS III scores and Levodopa equivalent daily dose (LEDD) were significantly decreased after DBS. However, in 17 patients who underwent both pre-and post-operative 99mTc-TRODAT-1 SPECT, no significant change was seen in any quantitative parameters, including right and left striatal-binding ratio (SBR) as well as striatal asymmetry index (SAI). No significant correlation was also found between the percent of UPDRS III change after DBS and values of preoperative SBRs. The percentage of LEDD reduction also showed no significant correlation with the preoperative state of 99 m-TRODAT-1 SPECT. CONCLUSION: Our results showed that the mechanism of DBS action is not accompanied by short-term compensation of DAT in basal ganglia in severely advanced PD.
AbstractJournal Article BOOK REVIEWS Get access Drugs for the Treatment of Parkinson's Disease, Handbook of Experimental Pharmacology, Volume 88. Edited by D. R. Calne . 1989. Pp. 599. Berlin: Springer. Price DM 480.00. Function and Dysfunction in the Basal Ganglia. Edited by A. J. Franks , J. W. Ironside, R. H. S. Mindham, R. J. Smith, E. G. S. Spokes and W. W. Winlow. 1990. Pp. 277. Manchester: Manchester University Press. Price £49.95. ANDREW LEES ANDREW LEES Search for other works by this author on: Oxford Academic PubMed Google Scholar Brain, Volume 113, Issue 5, October 1990, Pages 1584–1585, https://doi.org/10.1093/brain/113.5.1584 Published: 01 October 1990
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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