ArticleJournal of Alzheimer's disease : JAD2010
The KATP channel activator diazoxide ameliorates amyloid-β and tau pathologies and improves memory in the 3xTgAD mouse model of Alzheimer's disease.
Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- KFrontiers in neurology · 2024Pooled it
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Unlocking Neuroprotection: Potassium Channel Openers in Alzheimer's Disease.Current Alzheimer research · 2026Review
- Prioritizing repurposable drugs for Alzheimer's disease using network-based analysis with concurrent assessment of Long QT syndrome risk.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- Unraveling the Plausible Role of Potassium Channel Openers in Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2025Article
- Potential Alzheimer's early biomarkers in a transgenic rat model and benefits of diazoxide/dibenzoylmethane co-treatment on spatial memory and AD-pathology.Scientific reports · 2024Article
- Novel Strategies to Improve the Cardioprotective Effects of Cardioplegia.Current cardiology reviews · 2024Review
- Ion Channels and Ionotropic Receptors in Astrocytes: Physiological Functions and Alterations in Alzheimer's Disease and Glioblastoma.Life (Basel, Switzerland) · 2023Review
- Identification of Potential Repurposable Drugs in Alzheimer's Disease Exploiting a Bioinformatics Analysis.Journal of personalized medicine · 2022Article
- The 40-Hz White Light-Emitting Diode (LED) Improves the Structure-Function of the Brain Mitochondrial KATP Channel and Respiratory Chain Activities in Amyloid Beta Toxicity.Molecular neurobiology · 2022Article
- Somatostatin-evoked Aβ catabolism in the brain: Mechanistic involvement of α-endosulfine-KMolecular psychiatry · 2022Article
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- Kir6.2 is essential to maintain neurite features by modulating PM20D1-reduced mitochondrial ATP generation.Redox biology · 2021Article
- Routes for Potassium Ions across Mitochondrial Membranes: A Biophysical Point of View with Special Focus on the ATP-Sensitive KBiomolecules · 2021Review
- Phosphorylated tau targeted small-molecule PROTACs for the treatment of Alzheimer's disease and tauopathies.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Age-related impairment of cerebral blood flow response to KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Review
- Article
- Article
- Repeated electromagnetic field stimulation lowers amyloid-β peptide levels in primary human mixed brain tissue cultures.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Compromised cellular energy metabolism, cerebral hypoperfusion, and neuronal calcium dysregulation are involved in the pathological process of Alzheimer's disease (AD). ATP-sensitive potassium (KATP) channels in plasma membrane and inner mitochondrial membrane play important roles in modulating neuronal excitability, cell survival, and cerebral vascular tone. To investigate the therapeutic potential of drugs that activate KATP channels in AD, we first characterized the effects of the KATP channel opener diazoxide on cultured neurons, and then determined its ability to modify the disease process in the 3xTgAD mouse model of AD. Plasma and mitochondrial membrane potentials, cell excitability, intracellular Ca2+ levels and bioenergetics were measured in cultured cerebral cortical neurons exposed to diazoxide. Diazoxide hyperpolarized neurons, reduced the frequency of action potentials, attenuated Ca2+ influx through NMDA receptor channels, and reduced oxidative stress. 3xTgAD mice treated with diazoxide for 8 months exhibited improved performance in a learning and memory test, reduced levels of anxiety, decreased accumulation of Aβ oligomers and hyperphosphorylated tau in the cortex and hippocampus, and increased cerebral blood flow. Our findings show that diazoxide can ameliorate molecular, cytopathological, and behavioral alterations in a mouse model of AD suggesting a therapeutic potential for drugs that activate KATP channels in the treatment of 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.