DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for amnesia — screening already-approved drugs against its 18-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAmnesia maps to a 18-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 amnesia 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
gamma-aminobutyric acid type A receptor subunit alpha4 (GABRA4) — GABRA4 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 px6drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 7QN5 · 2.5 Å · ligand 1,2-DIPALMITOYL-SN-GLYCERO-3-PHOSPHATE (PX6). Experimental structure, not a prediction.
What the evidence adds up to
Two case reports from 2002 describe elderly men with sudden, permanent amnesia that could not be explained by stroke, hypoglycaemia, syncope, or seizure. One man, aged 80, lost memory of the previous 60 years; autopsy five years later showed Alzheimer disease. The other, aged 70, developed disabling amnesia overnight that did not progress over 15 years; MRI ten years after onset showed bilateral medial temporal lobe abnormality. The authors concluded that rare cases of amnesia may result from an unrecognised pathophysiological process.
A 2022 rat study tested the terpenoid carveol against scopolamine-induced memory impairment. Carveol at 50, 100, and 200 mg/kg reduced escape latency and increased time in the target quadrant in the Morris water maze, and increased spontaneous alternations and entries in the Y-maze. In brain tissue, carveol raised glutathione, glutathione-s-transferase, catalase, and lowered lipid peroxides. It also reduced expression of amyloid-beta, nuclear factor kappa-light-chain-enhancer of activated B cells, tumour necrosis factor-alpha, cyclooxygenase-2, prostaglandin E2, and interleukin-18. The authors concluded carveol might be potent against amnesia via antioxidant, amyloid-beta inhibition, and anti-inflammatory pathways. These results are from a single rodent model using scopolamine, not from human amnesia patients.
A 2021 systematic review of non-pharmacological interventions for post-traumatic amnesia after traumatic brain injury screened 1,036 articles and found eight eligible studies, four of which were randomised trials. Interventions included structured retraining of daily activities (four studies), reality orientation (two studies), the Perceive, Recall, Plan and Perform system (one study), and music therapy (one study). Seven of the eight studies reported positive or partially positive results. The review did not provide specific effect sizes or survival data.
A 2025 review of transient global amnesia, transient epileptic amnesia, and functional amnesia notes that no evidence-based therapeutic recommendations exist because the pathogenesis of transient global amnesia is not understood. The author suggests that if interventions to reactivate latent or silent engram neurones become available, they might have therapeutic implications, but no such interventions are described. A separate 2025 review lists potential treatment options including pharmaceutical intervention, neuromodulation, and gene therapy for mnemonic recovery, but provides no clinical trial data, response rates, or survival figures for any of these approaches in human amnesia.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Archives of Neurology · 2002 · 15 citations
Unexplained Sudden Amnesia
AbstractBACKGROUND: In almost all cases of acute, sudden, persistent amnesia, the cause can be determined. Ischemic stroke, hypoglycemia, syncope, and seizure are the most likely causes. PATIENTS AND METHODS: In a clinical study, 2 elderly men are described in which sudden, permanent amnesia developed in the absence of a satisfactory explanation. In 1 case, a neuropathologic study disclosed Alzheimer disease; in the other, magnetic resonance imaging showed a temporal lobe abnormality bilaterally. RESULTS: A man aged 80 years suddenly lost his memory of the previous 60 years. Neuropathologic study 5 years later showed the changes of Alzheimer disease. In the second case a disabling amnesia developed overnight in a man aged 70 years. There was no progression of the disabling amnesia in the next 15 years. Magnetic resonance imaging 10 years from the onset showed abnormality of the medial temporal lobe bilaterally. CONCLUSIONS: In neither case was the amnesia satisfactorily explained. It is likely that rare cases of amnesia occur as the result of an unrecognized pathophysiologic process.
Psychiatry Investigation · 2011 · 9 citations · open access
Use of Lorazepam in Drug-Assisted Interviews: Two Cases of Dissociative Amnesia
AbstractDrug-assisted interviews are useful for psychiatric diagnosis and treatment. However, amobarbital, a typical medication used for this purpose, is associated with elevated risk of respiratory depression. Benzodiazepines are good substitutes for amobarbital, with similar therapeutic effects and fewer complications. Although drug-assisted interviews are not widely used, they may be beneficial for selected patients who do not respond to conventional treatments such as supportive psychotherapy or psychopharmacotherapy. We report two cases of dissociative amnesia that were treated using lorazepam-assisted interviews. The use of lorazepam in drug-assisted interviews is effective and safe for resolving dissociative amnesia.
Ameliorative effect of carveol on scopolamine-induced memory impairment in rats.
AbstractObjectives: is a naturally occurring terpenoid with antispasmodic, carminative, astringent, indigestion, and dyspepsia properties, as well as anti-diabetic, anti-oxidant, anti-hyperlipidemia, and anti-inflammatory properties in the liver. Research also suggests that it has memory-enhancing and anti-oxidant properties. The purpose of this research was to see whether carveol could protect rats against scopolamine-induced memory loss in a rat model. Materials and Methods: <0.005 was considered statistically significant. Results: The in vitro assay showed that carveol caused diphenyl-1-picrylhydrazyl inhibition. In-vivo findings revealed that carveol (50, 100, and 200 mg/kg) significantly improved dementia by reducing escape latency and spending more time in the targeted quadrant in the Morris water maze test. Increased number of entries and percent spontaneous alterations were observed in rats' Y-maze test. In animal brain tissues, i.e., cortex and hippocampus, carveol enhanced glutathione, glutathione-s-transferase, catalase, and reduced lipid peroxide levels. Carveol also improved cellular architecture in histopathological examinations and decreased expression of inflammatory markers such as amyloid-beta, nuclear factor kappa light chain activated B cells, tumor necrosis factor-alpha, cyclooxygenase 2, prostaglandin E2, and interleukin-18, as evidenced by immunohistochemistry and enzyme-linked immunosorbent assays, as well as molecular investigations. Conclusion: This study suggests that the compound could be potent against amnesia mediated through anti-oxidant, amyloid-beta inhibition, and anti-inflammatory pathways.
Intervención no farmacológica en la amnesia postraumática, una revisión sistemática
AbstractINTRODUCTION: Survivors of traumatic brain injury may experience a transient state of confusion and global disturbance of cognitive-behavioural functioning called post-traumatic amnesia. AIM: To describe the characteristics, methodological quality and main results of studies that have analysed the impact of non-pharmacological interventions in the treatment of symptoms associated with post-traumatic amnesia. PATIENTS AND METHODS: Following the PRISMA guidelines, a literature search was carried out on papers published in the PubMed and PsycInfo databases over the last 20 years (2000-2020). The methodological quality of the articles was assessed using the PEDro scale. RESULTS: After applying the inclusion and exclusion criteria, of the 1,036 potentially interesting articles, eight met the eligibility criteria, four of which were randomised clinical trials. The interventions applied were grouped as follows: structured retraining of activities of daily living (four studies), reality orientation programme (two studies), Perceive, Recall, Plan and Perform system (one study) and therapeutic application of music (one study). Seven of the eight articles reviewed showed positive or partially positive results. CONCLUSIONS: According to the results obtained, there is evidence that non-pharmacological interventions have positive effects on reducing the cognitive-behavioural signs and symptoms associated with post-traumatic amnesia.
Neurology International · 2025 · 0 citations · open access
An “Engram-Centric” Approach to Transient Global Amnesia (TGA) and Other Acute-Onset Amnesias
AbstractThe differential diagnosis of acute-onset amnesia includes transient global amnesia (TGA), transient epileptic amnesia (TEA), and functional (or psychogenic) amnesia. The most common of these, TGA, is a rare but well-described condition characterised by a self-limited episode of dense anterograde amnesia with variable retrograde amnesia. Although the clinical phenomenology of TGA is well described, its pathogenesis is not currently understood, thus preventing the development of evidence-based therapeutic recommendations. Here, TGA, TEA, and functional amnesia are considered in light of the historical engram conception of memory, now informed by recent experimental research, as disturbances in distributed ensembles of engram neurones active during memory formation and recall. This analysis affords therapeutic implications for these conditions, should interventions to reactivate latent or silent engrams become available.
Zenodo (CERN European Organization for Nuclear Research) · 2025 · 0 citations · open access
DECODING AMNESIA: NEURAL MECHANISMS, ANIMAL MODELS, AND TRANSLATIONAL INSIGHTS
AbstractAmnesia is a multifactorial neurological disorder that is marked by loss in encoding, consolidation, and retrieving memories. This review examines the clinical subtypes of amnesia- such as anterograde, retrograde, transient global and dissociative amnesia-and the neural basis underlying these subtypes especially the hippocampus, medial temporal lobe and the network of associated cortices. We emphasize such important molecular processes as the disruption of synaptic plasticity, the neurotransmitter imbalance, and neuro inflammatory signalling. The animal models have played an invaluable role in explaining the pathophysiology of amnesia. CREB, BDNF, and NMDA receptor pathway models Chemically induced models (e.g., scopolamine, muscimol) and genetic manipulations have provided important understanding of the dysfunction of memory and therapeutic targets. Rodent and zebrafish models can be used to complement each other in the study of molecular cascades and behavioural phenotypes. The cross-species comparisons are highlighted in order to increase translational relevance, to make the difference between preclinical results and human clinical outcomes. New treatment options, such as pharmaceutical intervention, neuromodulation and gene therapy, are addressed in terms of mnemonic recovery. This review aim to cover the horizon of animal models used to study amnesia and its related complication.
Journal of Gastroenterology & Hepatology Reports · 2022 · 0 citations · open access
Wernicke’s Encephalopathy in the Setting of Severe Malnutrition and Alcohol Abuse
AbstractWernicke’s encephalopathy is an acute, potentially fatal syndrome attributable to thiamine deficiency. Prompt identification and treatment is essential to prevent the development of Korsakoff syndrome, an irreversible memory disorder associated with both retrograde and anterograde amnesia. Here, we present a case of a 39-year-old woman admitted to the ICU with a diagnosis of alcohol withdrawal and severe malnutrition. On admission, the patient was noted to have horizontal nystagmus and underwent aggressive thiamine repletion resulting in resolution of her symptoms.
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.
