DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for cerebral amyloid angiopathy — screening already-approved drugs against its 8-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCerebral amyloid angiopathy maps to a 8-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 cerebral amyloid angiopathy 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
apolipoprotein E (APOE) — APOE 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 8AX9 · 1.549 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
Fourteen patients with pathologically confirmed CAA-related inflammation were followed for an average of nearly four years. Seven of twelve with imaging and follow-up data had a monophasic improvement after immunosuppressive treatment, three improved initially then relapsed, and two showed no response at all. One patient had a symptomatic intracerebral haemorrhage inside a region of recurrent MRI hyperintensity. The APOE ε4/ε4 genotype was found in ten of thirteen subjects (76.9%) compared with two of thirty-nine (5.1%) patients who had non-inflammatory CAA, a statistically significant difference.
Cerebral amyloid angiopathy itself is a common cause of primary lobar intracerebral haemorrhage in elderly people, with frequent recurrence of bleeding and asymptomatic petechial haemorrhages. No specific secondary stroke prevention treatment exists for sporadic CAA. One 2021 review proposes tranexamic acid as a potential agent based on the fibrinolytic system’s interaction with amyloid, but this remains a hypothesis requiring further research.
A single case report describes a 38-year-old woman who had repeated intracerebral haemorrhages from CAA three decades after a cadaveric dural graft used to close an astrocytoma resection. Imaging showed extensive left parenchymal haematoma, multiple microbleeds, and superficial siderosis. Congo Red staining confirmed amyloid deposits in blood vessels. Genetic testing found no mutation linked to hereditary β-amyloid pathology.
Updated diagnostic criteria, the Boston 2.0 criteria, have been published for CAA, which presents with intracerebral haemorrhage and cognitive impairment in elderly patients. What remains missing is a proven treatment to prevent recurrent haemorrhage in sporadic CAA, adequate funding for clinical trials of candidate agents such as tranexamic acid, and better patient stratification by genotype and inflammatory subtype to guide any future therapy.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Neurology · 2007 · 333 citations
Course of cerebral amyloid angiopathy–related inflammation
AbstractBACKGROUND: A subset of patients with cerebral amyloid angiopathy (CAA) present with cognitive symptoms, seizures, headaches, T2-hyperintense MRI lesions, and neuropathologic evidence of CAA-associated vascular inflammation. OBJECTIVE: To analyze the risk factors, diagnostic characteristics, and long-term course of this disorder. METHODS: We assessed 14 consecutive patients with pathologically diagnosed CAA-related inflammation, 12 with available neuroimaging and follow-up data. Patients were evaluated for MRI appearance, APOE genotype, and clinical course over a 46.8 +/- 29.1-month follow-up. RESULTS: Baseline MRI scans were characterized by asymmetric T2-hyperintense lesions extending to the subcortical white matter and occasionally the overlying gray matter, with signal properties suggesting vasogenic edema. Subjects could be divided into three groups based on response to immunosuppressive treatment: monophasic improvement (7/12), initial improvement followed by symptomatic relapse (3/12), and no evident response to treatment (2/12). The volume of MRI hyperintensities correlated with the severity of clinical symptoms. One patient experienced symptomatic intracerebral hemorrhage within a region of recurrent MRI hyperintensity. The APOE epsilon4/epsilon4 genotype was strongly associated with CAA-related inflammation, present in 76.9% (10/13) of subjects vs 5.1% (2/39) with symptomatic but noninflammatory CAA (p < 0.0001). CONCLUSION: Cerebral amyloid angiopathy-related inflammation represents a clinically, pathologically, radiographically, and genetically distinct disease subtype with implications for clinical practice and ongoing immunotherapeutic approaches to Alzheimer disease.
Cerebral Amyloid Angiopathy and Lobar Intracerebral Hemorrhage
AbstractCerebral amyloid angiopathy is caused by the deposition of β-amyloid in the media and adventitia of small arteries and capillaries of the meninges and cerebral cortex. It is now recognized as a common cause of primary lobar intracerebral hemorrhage in elderly persons, and it is associated with frequent hemorrhage recurrence and the presence of asymptomatic petechial hemorrhages. Interestingly, although it has been nearly a century since the first pathological descriptions of cerebral amyloid angiopathy, knowledge of its link with intracerebral hemorrhage developed only within the last 35 years. This review provides a historical perspective on the still-evolving concept of cerebral amyloid angiopathy-related disease.
Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target?
AbstractCerebral amyloid angiopathy is a devastating cause of intracerebral hemorrhage for which there is no specific secondary stroke prevention treatment. Here we review the current literature regarding cerebral amyloid angiopathy pathophysiology and treatment, as well as what is known of the fibrinolytic pathway and its interaction with amyloid. We postulate that tranexamic acid is a potential secondary stroke prevention treatment agent in sporadic cerebral amyloid angiopathy, although further research is required.
Journal of Neurosurgery Research and Reviews · 2021 · 3 citations · open access
Early-Onset Cerebral Amyloid Angiopathy, A Prion-Like Disease: Case Report and Literature Review
AbstractWe report the case of a 38-year-old woman who suffered repeated intracerebral hemorrhages caused by cerebral amyloid angiopathy three decades after an astrocytoma resection with cadaveric dural graft used for closing. Neuroimaging showed extensive left parenchymal hematoma, several microbleeds and frontal and occipital superficial siderosis. Pathology showed blood vessels with deposits stained with Congo Red, suggestive of cerebral amyloid angiopathy. Genetic tests did not reveal any mutation related to hereditary forms of β -amyloid pathology.
Zenodo (CERN European Organization for Nuclear Research) · 2024 · 0 citations · open access
Boston 2.0 Criteria for Cerebral Amyloid Angiopathy
AbstractCerebral amyloid angiopathy is a common small vessel disease presenting in elderly patients involving amyloid-β deposition in the cerebral vasculature, contributing to intracerebral hemorrhage and cognitive impairment. Updated diagnostic criteria are essential for work-up and management.
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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