DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for brain disease — screening already-approved drugs against its 35-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleBrain disease maps to a 35-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 brain 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
chitinase 3 like 2 (CHI3L2) — CHI3L2 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 ndgdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4P8W · 1.87 Å · ligand 2-acetamido-2-deoxy-alpha-D-glucopyranose (NDG). Experimental structure, not a prediction.
What the evidence adds up to
A 2014 protocol paper for poor-grade subarachnoid haemorrhage, where mortality ranges from 34% to 52%, proposes combining multimodality monitoring with induced hypothermia to track inflammatory and neuroregenerative markers in blood and cerebrospinal fluid. The authors hypothesise that injury-induced neurogenesis might be a prognostic factor that can be monitored and modulated, but the paper presents no patient data, only a study design and expected outcomes. No results are reported, so no conclusion about efficacy can be drawn from this work.
A 2019 case report describes a 72-year-old woman with Crohn's disease who developed a progressive encephalopathy with bradypsychia and gait difficulty, culminating in coma, months after starting metronidazole. MRI showed hyperintensities in the corpus callosum, red nuclei and dentate nuclei; autopsy after her death from sepsis revealed cell necrosis and demyelination in the red nucleus. Stopping metronidazole produced clinical improvement before the fatal sepsis, and the authors frame the condition as a rare, treatable cause of subacute encephalopathy, but the evidence is a single case with a complicated terminal course.
A 2004 news item reports that the UK Academy of Medical Sciences called for faster translation of basic neuroscience research into patient benefit, arguing that treatments could shift from helping patients adapt to brain impairment towards promoting functional recovery. The piece contains no trial data. A 1970 journal notice and a 1983 book review offer no original evidence. A 2021 review on dyscirculatory encephalopathy summarises pathogenesis, staging and general therapeutic principles for the condition, but provides no quantitative outcomes.
A 2015 textbook preface notes that chemotherapy combined with other treatments has been established as effective for some brain cancers such as glioblastoma and CNS lymphoma, and that surgical and device treatments for epilepsy and pain have improved in safety and efficacy. It gives no specific response rates or survival figures. Across all these abstracts, there is no drug with demonstrated benefit for any brain disease; the only drug mentioned as a cause of encephalopathy is metronidazole. What is missing is any controlled trial, any patient stratification by biomarker or imaging phenotype, and any funding commitment to test the hypothermia-monitoring hypothesis or the neuroregeneration concept in humans.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Neurosurgery · 2014 · 21 citations · open access
Multimodality Monitoring, Inflammation, and Neuroregeneration in Subarachnoid Hemorrhage
AbstractBACKGROUND: Stroke, including subarachnoid hemorrhage (SAH), is one of the leading causes of morbidity and mortality worldwide. The mortality rate of poor-grade SAH ranges from 34% to 52%. In an attempt to improve SAH outcomes, clinical research on multimodality monitoring has been performed, as has basic science research on inflammation and neuroregeneration (which can occur due to injury-induced neurogenesis). Nevertheless, the current literature does not focus on the integrated study of these fields. Multimodality monitoring corresponds to physiological data obtained during clinical management by both noninvasive and invasive methods. Regarding inflammation and neuroregeneration, evidence suggests that, in all types of stroke, a proinflammatory phase and an anti-inflammatory phase occur consecutively; these phases affect neurogenesis, which is also influenced by other pathophysiological features of stroke, such as ischemia, seizures, and spreading depression. OBJECTIVE: To assess whether injury-induced neurogenesis is a prognostic factor in poor-grade SAH that can be monitored and modulated. METHODS: We propose a protocol for multimodality monitoring-guided hypothermia in poor-grade SAH in which cellular and molecular markers of inflammation and neuroregeneration can be monitored in parallel with clinical and multimodal data. EXPECTED OUTCOMES: This study may reveal correlations between markers of inflammation and neurogenesis in blood and cerebrospinal fluid, based on clinical and multimodality monitoring parameters. DISCUSSION: This protocol has the potential to lead to new therapies for acute, diffuse, and severe brain diseases.
Encefalopatía inducida por metronidazol: descripción de un caso con hallazgos radiológicos y anatomopatológicos
AbstractINTRODUCTION: Metronidazole is a widely known and used antibiotic. In exceptional cases, an encephalopathy with characteristic lesions on magnetic resonance imaging (MRI), usually located in the cerebellum and splenium of the corpus callosum, may be an adverse effect. The incidence and pathogenesis are unknown. The suspension of the treatment usually resolves the symptoms and normalizes the MRI in a few weeks. Due to the usual good prognosis, the anatomopathological findings are exceptional. We present a clinical case with the radiological findings suggestive of metronidazole-induced encephalopathy and, exceptionally, we provide the anatomopathological findings. CASE REPORT: A 72 years-old woman with severe Crohn's disease who, months after starting treatment with metronidazole, presented a slowly progressing bradypsychia and difficulty walking until she came to coma. In MRI it showed hyperintense images in T2 in the corpus callosum, red and dentate nuclei. He improved by stopping metronidazole but later developed sepsis and died. At autopsy, softening of the red nucleus was observed and, microscopically, cell necrosis and demyelination. CONCLUSION: With the publication of the clinical, radiological and anatomopathological information of our case we intend to promote the knowledge of this infrequent treatable cause of subacute encephalopathy and provide data that help to clarify its pathogenesis.
AbstractThe past few years have been extremely exciting for both neuroscientists and clinicians. We are unlocking the mysteries of the human mind and applying these discoveries to create better treatment for those affected with neurological disorders, leading to more effective therapies. A new patient-centered medicine approach will hopefully lead to fewer side effects and increased efficacy. This edition of Essential Neuropharmacology focuses on pharmacological treatment; however, substantial improvements in surgical and medical device treatments for neurological disorders have occurred. These include surgical treatments for epilepsy, deep brain stimulation, transcranial magnetic stimulation, vagal nerve stimulation, and occipital and other nerve stimulators for pain. Due to improvements in safety and proven efficacy, some of these procedures may now be considered earlier, rather than as a last resort. Given the expanding role of neurologists, we also decided to widen the focus of the textbook to include areas such as sleep and neuro-oncology. The practice of sleep medicine has expanded and chemotherapy has been established as effective when combined with other treatments for the treatment of some brain cancers, such as glioblastoma and CNS lymphoma, and neurologists increasingly are working with neurosurgeons and radiation oncologists to manage these challenging disorders. Like most neurologists, we became interested in neurology due to our fascination with the nervous system and by the fact that there is so much more to learn. The scope of neurological practice continues to expand, with increasing degrees of specialization. Although we practice based on available evidence, often we must revert to trial and error for our difficult cases. Keeping track of the newest medications and developments in our expanding field is a challenge. We have all had the experience of running into a complicated patient, and we know how important it is to discuss the case with an expert. We hope that this text will help those who don't have immediate access to such expertise and will lead to better care for patients with neurological disorders.
UK academy wants neuroscience research to benefit patients more quickly
AbstractThe Academy of Medical Sciences in the United Kingdom has called for more rapid translation of basic research in neuroscience to better management and patient care for patients with neurological diseases.
In a report published this week, the academy suggests that an opportunity exists to move from current treatments that primarily help patients with neurological conditions suchas Alzheimer's disease, stroke, and cerebral palsy to adapt to their brain impairment to a new era that focuses on helping the brain to achieve a measure of functional recovery. It argued that increased investment in research into diseases of the brain was offering the potential to develop treatments that would reduce the …
AbstractJournal Article NOTICES OF RECENT PUBLICATIONS Get access Therapy for Neurologic Disorders. Edited by W. C. Wiederholt. 1982. Pp. 437. Chichester: John Wiley. Price £35.00. DONALD B. CALNE DONALD B. CALNE Search for other works by this author on: Oxford Academic PubMed Google Scholar Brain, Volume 106, Issue 2, June 1983, Page 527, https://doi.org/10.1093/brain/106.2.527 Published: 01 June 1983
Postgraduate Medical Journal · 1970 · 0 citations · open access
Iatrogenic encephalopathy
AbstractJournal Article Iatrogenic encephalopathy. Get access P Monro, B.Sc., M.D., M.R.C.P P Monro, B.Sc., M.D., M.R.C.P Atkinson Morley’s Hospital, Copse Hill, Wimbledon, London, S.W.20 Search for other works by this author on: Oxford Academic Google Scholar Postgraduate Medical Journal, Volume 46, Issue 535, May 1970, Pages 327–329, https://doi.org/10.1136/pgmj.46.535.327 Published: 01 May 1970
Spravočnik vrača obŝej praktiki (Journal of Family Medicine) · 2021 · 0 citations
Dyscirculatory encephalopathy in the practice of a family doctor
AbstractThe article highlights the issues related to the development of dyscirculatory encephalopathy (DE), in particular, against the background of what diseases this pathology occurs and its social significance. The main issues of its pathogenesis are considered; the parts of the brain that are damaged in the first place and how this affects the manifestations of the disease and the rate of its development are described. The staging of DE development, the main symptoms and problems of its diagnosis are also considered. The basic principles of therapy are presented: the indications for inpatient and outpatient treatment, groups of drugs used to improve the patient’s condition and the mechanisms of their action.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works using Disease Ontology synonyms, resolved on OpenAlex.
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