His primary scientific interests are in Epilepsy, Pediatrics, Internal medicine, Paroxysmal dyskinesia and Mutation. Neuroscience covers Holger Lerche research in Epilepsy. His studies deal with areas such as Hippocampal sclerosis, Temporal lobe and Age of onset as well as Pediatrics.
The various areas that Holger Lerche examines in his Temporal lobe study include Surgery, Neuropathology, Disease and Epilepsy surgery. As a part of the same scientific family, Holger Lerche mostly works in the field of Internal medicine, focusing on Endocrinology and, on occasion, Generalized epilepsy with febrile seizures plus. Holger Lerche combines subjects such as Cytoplasmic part, Cytoplasm and Binding site with his study of Mutation.
His primary areas of study are Epilepsy, Neuroscience, Genetics, Internal medicine and Mutation. Within one scientific family, Holger Lerche focuses on topics pertaining to Missense mutation under Epilepsy, and may sometimes address concerns connected to Generalized epilepsy. Electrophysiology, Temporal lobe, Electroencephalography, Hippocampus and Dravet syndrome are among the areas of Neuroscience where Holger Lerche concentrates his study.
His work deals with themes such as Juvenile myoclonic epilepsy and Rolandic epilepsy, which intersect with Genetics. Holger Lerche has included themes like Gastroenterology and Endocrinology in his Internal medicine study. His Mutation research is multidisciplinary, incorporating elements of Mutant and Cell biology.
Epilepsy, Neuroscience, Phenotype, Internal medicine and Missense mutation are his primary areas of study. Holger Lerche is interested in Generalized epilepsy, which is a branch of Epilepsy. His study in the field of Electrophysiology, Thalamus and Electroencephalography also crosses realms of Clinical neurology.
He interconnects Mutation and Mutant in the investigation of issues within Phenotype. His Internal medicine research is multidisciplinary, relying on both Gastroenterology and Endocrinology. His work carried out in the field of Missense mutation brings together such families of science as Sodium channel blocker, Loss function, Gating and Dravet syndrome.
Holger Lerche mainly focuses on Epilepsy, Phenotype, Missense mutation, Genetics and Intellectual disability. His research integrates issues of Mutation, Computational biology and Cohort study in his study of Epilepsy. The study incorporates disciplines such as Electrophysiology, Signal transducing adaptor protein and Bioinformatics in addition to Phenotype.
The various areas that he examines in his Missense mutation study include SCN3A, Nonsense, Dravet syndrome, Copy-number variation and Sodium channel blocker. His Genetics study combines topics from a wide range of disciplines, such as Ataxia, Myoclonus and Disinhibition. The Intellectual disability study combines topics in areas such as Autism, Neuroscience and Episodic ataxia.
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Analysis of shared heritability in common disorders of the brain
Verneri Anttila;Verneri Anttila;Brendan Bulik-Sullivan;Brendan Bulik-Sullivan;Hilary K. Finucane;Raymond K. Walters;Raymond K. Walters.
Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): A retrospective study
Philippe Ryvlin;Lina Nashef;Samden D Lhatoo;Lisa M Bateman.
Lancet Neurology (2013)
Histopathological Findings in Brain Tissue Obtained during Epilepsy Surgery.
Blumcke I;Spreafico R;Haaker G;Coras R.
The New England Journal of Medicine (2017)
Mutations in GRIN2A cause idiopathic focal epilepsy with rolandic spikes
Johannes R Lemke;Dennis Lal;Eva M Reinthaler;Isabelle Steiner.
Nature Genetics (2013)
GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak
Yvonne G. Weber;Alexander Storch;Thomas V. Wuttke;Knut Brockmann.
Journal of Clinical Investigation (2008)
Paroxysmal exercise-induced dyskinesia and epilepsy is due to mutations in SLC2A1, encoding the glucose transporter GLUT1.
Arvid Suls;Peter Dedeken;Karolien Goffin;Hilde Van Esch.
Genetic and phenotypic heterogeneity suggest therapeutic implications in SCN2A-related disorders.
Markus Wolff;Katrine M Johannesen;Ulrike B S Hedrich;Silvia Masnada.
Eryptosis, a Window to Systemic Disease
Florian Lang;Erich Gulbins;Holger Lerche;Stephan M. Huber.
Cellular Physiology and Biochemistry (2008)
The new anticonvulsant retigabine favors voltage-dependent opening of the Kv7.2 (KCNQ2) channel by binding to its activation gate.
Thomas V. Wuttke;Guiscard Seebohm;Sigrid Bail;Snezana Maljevic.
Molecular Pharmacology (2005)
Efficacy and safety of adjunctive ezogabine (retigabine) in refractory partial epilepsy
M.J. Brodie;H. Lerche;A. Gil-Nagel;C. Elger.
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