ArticleBrain research2012
Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency.
Article in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 48 citations in OpenAlex.
- Dexpramipexole alleviates chronic allodynia from sciatic neuropathy and reduces spinal interferon-γ and other proinflammatory cytokines in spinal cord and dorsal root ganglia in mice.Medical research archives · 2026Article
- Reversing Mitochondrial Dysfunction in Optineurin E50K Glaucoma: A Metabolic Approach to Neuroprotection.Research square · 2026Article
- The FDA-approved compound, pramipexole and the clinical-stage investigational drug, dexpramipexole, reverse chronic allodynia from sciatic nerve damage in mice, and alter IL-1β and IL-10 expression from immune cell culture.Neuroscience letters · 2023Article
- Site-specific mitochondrial dysfunction in neurodegeneration.Mitochondrion · 2022Article
- Dexpramipexole Attenuates White Matter Injury to Facilitate Locomotion and Motor Coordination Recovery via Reducing Ferroptosis after Intracerebral Hemorrhage.Oxidative medicine and cellular longevity · 2022Article
- Dexpramipexole Enhances KMolecular neurobiology · 2021Article
- The multi-functional RNA-binding protein G3BP1 and its potential implication in neurodegenerative disease.Journal of neurochemistry · 2021Review
- Neuroprotection induced by dexpramipexole delays disease progression in a mouse model of progressive multiple sclerosis.British journal of pharmacology · 2020Article
- Parkinson's disease protein DJ-1 regulates ATP synthase protein components to increase neuronal process outgrowth.Cell death & disease · 2019Article
- Energy metabolism in ALS: an underappreciated opportunity?Acta neuropathologica · 2018Review
- Dexpramipexole improves bioenergetics and outcome in experimental stroke.British journal of pharmacology · 2018Article
- Implications of white matter damage in amyotrophic lateral sclerosis (Review).Molecular medicine reports · 2017Review
- Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments.Frontiers in neuroscience · 2016Review
- The mitochondrial complex V-associated large-conductance inner membrane current is regulated by cyclosporine and dexpramipexole.Molecular pharmacology · 2015Article
- Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target?British journal of pharmacology · 2014Review
- GNX-4728, a novel small molecule drug inhibitor of mitochondrial permeability transition, is therapeutic in a mouse model of amyotrophic lateral sclerosis.Frontiers in cellular neuroscience · 2014Article
- Article
- Mitochondrial protectant pramipexole prevents sex-specific long-term cognitive impairment from early anaesthesia exposure in rats.British journal of anaesthesia · 2013Article
- Mechanisms, models and biomarkers in amyotrophic lateral sclerosis.Amyotrophic lateral sclerosis & frontotemporal degeneration · 2013Review
- The elusive magic pill: finding effective therapies for mitochondrial disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Cellular stress or injury can result in mitochondrial dysfunction, which has been linked to many chronic neurological disorders including amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD). Stressed and dysfunctional mitochondria exhibit an increase in large conductance mitochondrial membrane currents and a decrease in bioenergetic efficiency. Inefficient energy production puts cells, and particularly neurons, at risk of death when energy demands exceed cellular energy production. Here we show that the candidate ALS drug dexpramipexole (DEX; KNS-760704; ((6R)-4,5,6,7-tetrahydro-N6-propyl-2,6-benzothiazole-diamine) and cyclosporine A (CSA) inhibited increases in ion conductance in whole rat brain-derived mitochondria induced by calcium or treatment with a proteasome inhibitor, although only CSA inhibited calcium-induced permeability transition in liver-derived mitochondria. In several cell lines, including cortical neurons in culture, DEX significantly decreased oxygen consumption while maintaining or increasing production of adenosine triphosphate (ATP). DEX also normalized the metabolic profile of injured cells and was protective against the cytotoxic effects of proteasome inhibition. These data indicate that DEX increases the efficiency of oxidative phosphorylation, possibly by inhibition of a CSA-sensitive mitochondrial conductance.
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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.