Associated Papers
Shared genetics in epilepsy and migraine: A scoping review.
Sahu P et al.
Epileptic Disorders : International Epilepsy Journal With Videotape, 2025
Mechanisms underlying CSD initiation implicated by genetic mouse models of migraine.
Pietrobon D et al.
The Journal of Headache and Pain, 2025
Unravelling the Genetic Landscape of Hemiplegic Migraine: Exploring Innovative Strategies and Emerging Approaches.
Alfayyadh MM et al.
Genes, 2024
Voltage-Gated Sodium Channel Dysfunctions in Neurological Disorders.
Barbieri R et al.
Life (basel, Switzerland), 2023
Idealized multiple-timescale model of cortical spreading depolarization initiation and pre-epileptic hyperexcitability caused by NaV1.1/SCN1A mutations.
Lemaire L et al.
Journal of Mathematical Biology, 2023
SCN1A channelopathies: Navigating from genotype to neural circuit dysfunction.
Bryson A et al.
Frontiers in Neurology, 2023
Gene variant effects across sodium channelopathies predict function and guide precision therapy.
Brunklaus A et al.
Brain : a Journal of Neurology, 2022
The gain of function SCN1A disorder spectrum: novel epilepsy phenotypes and therapeutic implications.
Brunklaus A et al.
Brain : a Journal of Neurology, 2022
The effect of alterations of schizophrenia-associated genes on gamma band oscillations.
Metzner C et al.
Schizophrenia (heidelberg, Germany), 2022
Initiation of migraine-related cortical spreading depolarization by hyperactivity of GABAergic neurons and NaV1.1 channels.
Chever O et al.
The Journal of Clinical Investigation, 2021
Hyperexcitable interneurons trigger cortical spreading depression in an Scn1a migraine model.
Auffenberg E et al.
The Journal of Clinical Investigation, 2021
Sodium channelopathies of skeletal muscle and brain.
Mantegazza M et al.
Physiological Reviews, 2021
Epilepsy and Migraine Shared Genetic and Molecular Mechanisms: Focus on Therapeutic Strategies.
Gotra P et al.
Molecular Neurobiology, 2021
Modeling NaV1.1/SCN1A sodium channel mutations in a microcircuit with realistic ion concentration dynamics suggests differential GABAergic mechanisms leading to hyperexcitability in epilepsy and hemiplegic migraine.
Lemaire L et al.
Plos Computational Biology, 2021
Deciphering in silico the Role of Mutated Na V 1.1 Sodium Channels in Enhancing Trigeminal Nociception in Familial Hemiplegic Migraine Type 3.
Suleimanova A et al.
Frontiers in Cellular Neuroscience, 2021
SCN1A Mutation-Beyond Dravet Syndrome: A Systematic Review and Narrative Synthesis.
Ding J et al.
Frontiers in Neurology, 2021
A Study among the Genotype, Functional Alternations, and Phenotype of 9 SCN1A Mutations in Epilepsy Patients.
Kluckova D et al.
Scientific Reports, 2020
SCN1A variants from bench to bedside-improved clinical prediction from functional characterization.
Brunklaus A et al.
Human Mutation, 2020
SCN1A/NaV 1.1 channelopathies: Mechanisms in expression systems, animal models, and human iPSC models.
Mantegazza M et al.
Epilepsia, 2019
Late sodium current blocker GS967 inhibits persistent currents induced by familial hemiplegic migraine type 3 mutations of the SCN1A gene.
Barbieri R et al.
The Journal of Headache and Pain, 2019
Advances in genetics of migraine.
Sutherland HG et al.
The Journal of Headache and Pain, 2019
Alterations in Schizophrenia-Associated Genes Can Lead to Increased Power in Delta Oscillations.
Mäki-Marttunen T et al.
Cerebral Cortex (new York, N.y. : 1991), 2019
Mouse Models of Familial Hemiplegic Migraine for Studying Migraine Pathophysiology.
Dehghani A et al.
Current Neuropharmacology, 2019
Dysfunctional Nav1.5 channels due to SCN5A mutations.
Han D et al.
Experimental Biology and Medicine (maywood, N.j.), 2018
Epilepsy in hemiplegic migraine: Genetic mutations and clinical implications.
Prontera P et al.
Cephalalgia : an International Journal of Headache, 2018
Gain of Function for the SCN1A/hNav1.1-L1670W Mutation Responsible for Familial Hemiplegic Migraine.
Dhifallah S et al.
Frontiers in Molecular Neuroscience, 2018
Pleiotropic effects of schizophrenia-associated genetic variants in neuron firing and cardiac pacemaking revealed by computational modeling.
Mäki-Marttunen T et al.
Translational Psychiatry, 2017
A novel SCN1A mutation identified in a Chinese family with familial hemiplegic migraine: A case report.
Zhang Y et al.
Cephalalgia : an International Journal of Headache, 2017
ExACtly zero or once: A clinically helpful guide to assessing genetic variants in mild epilepsies.
Bennett CA et al.
Neurology. Genetics, 2017
Genetics of Migraine: Insights into the Molecular Basis of Migraine Disorders.
Sutherland HG et al.
Headache, 2017
The genetic relationship between epilepsy and hemiplegic migraine.
Huang Y et al.
Neuropsychiatric Disease and Treatment, 2017
Early-onset familial hemiplegic migraine due to a novel SCN1A mutation.
Fan C et al.
Cephalalgia : an International Journal of Headache, 2016
Functional Effects of Schizophrenia-Linked Genetic Variants on Intrinsic Single-Neuron Excitability: A Modeling Study.
Mäki-Marttunen T et al.
Biological Psychiatry. Cognitive Neuroscience and Neuroimaging, 2016
The Revolution in Migraine Genetics: From Aching Channels Disorders to a Next-Generation Medicine.
Pellacani S et al.
Frontiers in Cellular Neuroscience, 2016
Rescuable folding defective NaV1.1 (SCN1A) mutants in epilepsy: properties, occurrence, and novel rescuing strategy with peptides targeted to the endoplasmic reticulum.
Bechi G et al.
Neurobiology of Disease, 2015
Two novel SCN1A mutations identified in families with familial hemiplegic migraine.
Weller CM et al.
Cephalalgia : an International Journal of Headache, 2014
Familial hemiplegic migraine due to L263V SCN1A mutation: discordance for epilepsy between two kindreds from Douro Valley.
Barros J et al.
Cephalalgia : an International Journal of Headache, 2014
Linking a genetic defect in migraine to spreading depression in a computational model.
Dahlem MA et al.
Peerj, 2014
Nonfunctional NaV1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defects.
Cestèle S et al.
Proceedings of the National Academy of Sciences of the United States of America, 2013
Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate.
Cox HC et al.
The Journal of Headache and Pain, 2011
Ranolazine selectively blocks persistent current evoked by epilepsy-associated Naν1.1 mutations.
Kahlig KM et al.
British Journal of Pharmacology, 2010