ArticleNature aging2021
Experimental and real-world evidence supporting the computational repurposing of bumetanide for
Article in Nature aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT06052163 (Phase IIa, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Evaluate the Safety and Tolerability of Bumetanide in Patients With Alzheimer's Disease.), which is not on this map. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Phase IIa, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Evaluate the Safety and Tolerability of Bumetanide in Patients With Alzheimer's Disease.
Who cites it
67 citing papers in PubMed, 107 citations in OpenAlex.
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- Integrating genetically predicted transcriptomic signatures with longitudinal real-world data enables scalable drug repurposing for Alzheimer's disease.Research square · 2026Article
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- From In Silico Hypothesis to Validation: The Role of Real-World Evidence in the Preliminary Verification of AI-Generated Drug-Repositioning Candidates: A Comprehensive Review.Journal of clinical medicine · 2026Review
- Inhibition of MAPK p38α overcomes the cancer immunosurveillance defect caused by FPR1 loss-of-function mutation.Cell reports. Medicine · 2026Article
- Network pharmacology-based discovery and experimental validation of novel drug repurposing candidates in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Computational discovery of precision therapeutics for hidradenitis suppurativa.bioRxiv : the preprint server for biology · 2026Article
- Chemo-omic pipeline enables discovery of prion synaptotoxic pathways and inhibitory drugs.bioRxiv : the preprint server for biology · 2026Article
- Synthesis of new sulfoximines and sulfonimidamides derivatives as NKCC1 inhibitors.Frontiers in chemistry · 2026Article
- Artificial Intelligence to Guide Repurposing of Drugs.Annual review of medicine · 2026Review
- A computational genetic- and transcriptomics-based study nominates drug repurposing candidates for the treatment of chronic pain.EBioMedicine · 2025Article
- Tailoring MAPK Pathways: New Therapeutic Avenues for Treating Alzheimer's Disease.Molecular neurobiology · 2025Review
- Article
- A computational medicine framework integrating multi-omics, systems biology, and artificial neural networks for Alzheimer's disease therapeutic discovery.Acta pharmaceutica Sinica. B · 2025Article
- Cerulenin partially corrects the disrupted developmental transcriptomic signature in Huntington's disease striatal medium spiny neurons.Stem cells (Dayton, Ohio) · 2025Article
- Integrated Computational and Functional Screening Identifies G9a Inhibitors for SETD2-mutant Leukemia.Genomics, proteomics & bioinformatics · 2025Article
- Drug repurposing for Alzheimer's disease and other neurodegenerative disorders.Nature communications · 2025Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
26 authors at 3 institutions in 1 country.
Funding
Abstract
The evident genetic, pathological, and clinical heterogeneity of Alzheimer's disease (AD) poses challenges for traditional drug development. We conducted a computational drug repurposing screen for drugs to treat apolipoprotein (apo) E4-related AD. We first established apoE-genotype-dependent transcriptomic signatures of AD by analyzing publicly-available human brain database. We then queried these signatures against the Connectivity Map database containing transcriptomic perturbations of >1300 drugs to identify those that best reverse apoE-genotype-specific AD signatures. Bumetanide was identified as a top drug for apoE4 AD. Bumetanide treatment of apoE4 mice without or with Aβ accumulation rescued electrophysiological, pathological, or cognitive deficits. Single-nucleus RNA-sequencing revealed transcriptomic reversal of AD signatures in specific cell types in these mice, a finding confirmed in apoE4-iPSC-derived neurons. In humans, bumetanide exposure was associated with a significantly lower AD prevalence in individuals over the age of 65 in two electronic health record databases, suggesting effectiveness of bumetanide in preventing AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.