ArticleBiology2023
ABC Transporter C1 Prevents Dimethyl Fumarate from Targeting Alzheimer's Disease.
Article in Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- The ABC transporter A7 modulates neuroinflammation via NLRP3 inflammasome in Alzheimer's disease mice.Alzheimer's research & therapy · 2025Article
- Diverse Efficacy of Dimethyl Fumarate in Alleviating the Late Streptozotocin-Induced Cognitive Impairment and Neuropathological Features in Rat.Molecular neurobiology · 2024Article
- Computer-aided pattern scoring (C@PS): a novel cheminformatic workflow to predict ligands with rare modes-of-action.Journal of cheminformatics · 2024Article
- ABCC1 Is a ΔNp63 Target Gene Overexpressed in Squamous Cell Carcinoma.International journal of molecular sciences · 2024Article
- Computer-aided pattern scoring - A multitarget dataset-driven workflow to predict ligands of orphan targets.Scientific data · 2024Article
- Dimethyl fumarate improves cognitive impairment and neuroinflammation in mice with Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Apolar Extracts of St. John's Wort Alleviate the Effects of β-Amyloid Toxicity in Early Alzheimer's Disease.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 5 countries.
Funding
Abstract
Alzheimer's disease (AD), the leading cause of dementia, is a growing health issue with very limited treatment options. To meet the need for novel therapeutics, existing drugs with additional preferred pharmacological profiles could be recruited. This strategy is known as 'drug repurposing'. Here, we describe dimethyl fumarate (DMF), a drug approved to treat multiple sclerosis (MS), to be tested as a candidate for other brain diseases. We used an APP-transgenic model (APPtg) of senile β-amyloidosis mice to further investigate the potential of DMF as a novel AD therapeutic. We treated male and female APPtg mice through drinking water at late stages of β-amyloid (Aβ) deposition. We found that DMF treatment did not result in modulating effects on Aβ deposition at this stage. Interestingly, we found that glutathione-modified DMF interacts with the ATP-binding cassette transporter ABCC1, an important gatekeeper at the blood-brain and blood-plexus barriers and a key player for Aβ export from the brain. Our findings suggest that ABCC1 prevents the effects of DMF, which makes DMF unsuitable as a novel therapeutic drug against AD. The discovered effects of ABCC1 also have implications for DMF treatment of multiple sclerosis.
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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 Socratic graph.