TOWARD THE MOLECULAR MECHANISM OF EARLY-ONSET EPILEPSY

早发性癫痫的分子机制

• 批准号: 8033877
• 负责人: MARK LEPPERT
• 金额: $ 50万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-12-01 至 2012-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8033877
• 关键词: 16q; Accidents; Adult; Affect; Alleles; Anticonvulsants; Antiepileptic Agents; Antiepileptogenic; Arts; Bacterial Toxins; Basic Science; Benign; Biological; Biological Availability; Child; Childhood; Chromosomes; Chromosomes, Human, Pair 8; Clinical Trials; Collaborations; Complex; Convulsions; Defect; Development; Diagnosis; Disease; Drug Delivery Systems; Electroencephalography; Environment; Epilepsy; Epileptogenesis; Etiology; Event; Familial benign neonatal epilepsy; Family; Family member; Febrile Convulsions; Fever; Gene Mutation; Genes; Genetic; Genetic Predisposition to Disease; Genetic Variation; Genome; Goals; Grant; Histology; Individual; Infection; Inherited; Intractable Epilepsy; Knock-in Mouse; Laboratories; Lead; Lesion; Lipopolysaccharides; Mediator of activation protein; Medical; Methodology; Methods; Missense Mutation; Modeling; Modification; Molecular; Mouse Strains; Mus; Mutate; Mutation; NR4A1 gene; Neurologist; Pathway interactions; Patient Care; Patients; Pharmaceutical Preparations; Phenotype; Potassium Channel; Predisposition; Process; Protein Subunits; Proteins; Refractory; Reporting; Research; Resistance; Role; Seizures; Staging; Susceptibility Gene; Synapses; Syndrome; Temporal Lobe Epilepsy; Therapeutic; Toxic effect; Translating; Trauma; Universities; Utah; Veterans; War; Work; base; behavior measurement; congenic; drug development; early childhood; early onset; gene discovery; infancy; innovation; insight; mouse model; mutant; neural circuit; new therapeutic target; next generation; novel; response