Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The ATP-sensitive K channel is seizure protective and required for effective dietary therapy in a model of mitochondrial encephalomyopathy.

Journal of neurogenetics - 1 Jan 2000

Fogle Keri J, Hertzler J Ian, Shon Joy H, Palladino Michael J

Abstract excerpt

Effective therapies are lacking for mitochondrial encephalomyopathies (MEs). MEs are devastating diseases that predominantly affect the energy-demanding tissues of the nervous system and muscle, causing symptoms such as seizures, cardiomyopathy, and neuro- and muscular degeneration. Even common anti-epileptic drugs which are frequently successful in ameliorating seizures in other diseases tend to have a lower...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Caloric Restriction
Share to Diet, Ketogenic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Disease Models, Animal

Share to Drosophila Proteins

Share to Mitochondrial Encephalomyopathies

Share to Mitochondrial Proton-Translocating ATPases

Share to Potassium Channels

Share to Seizures

Source

Open in PubMed Open full text

Identifiers

PMID: 27868454
DOI: 10.1080/01677063.2016.1252765
PMCID: PMC5590012

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The ATP-sensitive K channel is seizure protective and required for effective dietary therapy in a model of mitochondrial encephalomyopathy.PMID 27868454Read ↗

Oxidative stress and neuronal alteration: Mitochondrial dysfunction as a key player in intractable epilepsy - a narrative review.Semantic proximity Read ↗

Epilepsy in Mitochondrial Diseases—Current State of Knowledge on Aetiology and TreatmentSemantic proximity Read ↗

Mitochondrial dysfunction in epilepsy.Semantic proximity Read ↗

Differential effects of mTOR inhibition and dietary ketosis in a mouse model of subacute necrotizing encephalomyelopathySemantic proximity Read ↗

Metabolic aspects of genetic ion channel epilepsies.Semantic proximity Read ↗

Mitochondrial Energetics and TherapeuticsSemantic proximity Read ↗

Ketogenic Diet in Neuromuscular and Neurodegenerative DiseasesSemantic proximity Read ↗

Neuropathology in Drosophila mutants with increased seizure susceptibility.Semantic proximity Read ↗

Epilepsy in mitochondrial disorders.Semantic proximity Read ↗

Calorie Restriction Induces Degeneration of Neurons with Mitochondrial DNA Depletion by Altering ER-Mitochondria Calcium TransferSemantic proximity Read ↗

Muscle KATP channels: recent insights to energy sensing and myoprotection.Semantic proximity Read ↗

Oxidative Stress, Mitochondrial Dysfunction, and EpilepsySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.