ArticleHuman molecular genetics2011
Meclizine is neuroprotective in models of Huntington's disease.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
The trial behind it
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Bioenergetic reprogramming of macrophages reduces drug tolerance in Mycobacterium tuberculosis.Nature communications · 2025Article
- Meclizine rescues cardiac function and mitochondrial ultrastructure by ATP- and glycolysis-independent mechanisms in a genetic model of mitochondrial energy dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- Mechanism of Action and Translational Potential of (Stroke · 2024Article
- Neurodegenerative Diseases: New Hopes and Perspectives.Current molecular medicine · 2024Review
- Meclizine moderates lipopolysaccharide-induced neuroinflammation in mice through the regulation of AKT/ NF-κβ/ERK/JNK signaling pathway.Metabolic brain disease · 2023Article
- Nutritional and Behavioral Countermeasures as Medication Approaches to Relieve Motion Sickness: A Comprehensive Review.Nutrients · 2023Review
- Novel mTORC1 Inhibitors Kill Glioblastoma Stem Cells.Pharmaceuticals (Basel, Switzerland) · 2020Article
- SK channel-mediated metabolic escape to glycolysis inhibits ferroptosis and supports stress resistance in C. elegans.Cell death & disease · 2020Article
- Therapeutic Advances for Huntington's Disease.Brain sciences · 2020Review
- Impact of pharmacological agents on mitochondrial function: a growing opportunity?Biochemical Society transactions · 2019Review
- New directions in therapeutics for Huntington disease.Future neurology · 2018Review
- Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage.Molecular neurobiology · 2017Article
- Meclizine Prevents Ovariectomy-Induced Bone Loss and Inhibits Osteoclastogenesis Partially by Upregulating PXR.Frontiers in pharmacology · 2017Article
- Augmentation of glycolytic metabolism by meclizine is indispensable for protection of dorsal root ganglion neurons from hypoxia-induced mitochondrial compromise.Free radical biology & medicine · 2016Article
- Meclizine-induced enhanced glycolysis is neuroprotective in Parkinson disease cell models.Scientific reports · 2016Article
- Activation of SK2 channels preserves ER Ca²⁺ homeostasis and protects against ER stress-induced cell death.Cell death and differentiation · 2016Article
- Xyloketal-derived small molecules show protective effect by decreasing mutant Huntingtin protein aggregates in Caenorhabditis elegans model of Huntington's disease.Drug design, development and therapy · 2016Article
- Studying polyglutamine diseases in Drosophila.Experimental neurology · 2015Review
- Unraveling protein misfolding diseases using model systems.Future science OA · 2015Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Defects in cellular energy metabolism represent an early feature in a variety of human neurodegenerative diseases. Recent studies have shown that targeting energy metabolism can protect against neuronal cell death in such diseases. Here, we show that meclizine, a clinically used drug that we have recently shown to silence oxidative metabolism, suppresses apoptotic cell death in a murine cellular model of polyglutamine (polyQ) toxicity. We further show that this protective effect extends to neuronal dystrophy and cell death in Caenorhabditis elegans and Drosophila melanogaster models of polyQ toxicity. Meclizine's mechanism of action is not attributable to its anti-histaminergic or anti-muscarinic activity, but rather, strongly correlates with its ability to suppress mitochondrial respiration. Since meclizine is an approved drug that crosses the blood-brain barrier, it may hold therapeutic potential in the treatment of polyQ toxicity disorders, such as Huntington's disease.
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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.