Associated Papers
The astrocytic engine: Na+,K+-ATPase at the nexus of brain function and malfunction.
Verkhratsky A et al.
American Journal of Physiology. Cell Physiology, 2026
Abnormal neurovascular coupling induces glymphatic dysfunction in a mouse model of familial hemiplegic migraine type 2.
Duan C et al.
The Journal of Headache and Pain, 2025
The Quaternary Structure of the Sodium Pump Regulatory Complex Is Altered by Mutations of a Site Associated with Familial Hemiplegic Migraine.
Seflova J et al.
Molecular Neurobiology, 2025
Mechanisms underlying CSD initiation implicated by genetic mouse models of migraine.
Pietrobon D et al.
The Journal of Headache and Pain, 2025
Clinical characterization of a novel ATP1A2 p.Gly615Glu mutation in nine family members with familial hemiplegic migraine.
Romozzi M et al.
Brain Communications, 2025
Spontaneous spreading depolarizations originate subcortically in a novel mouse model of familial hemiplegic migraine type 2.
Jansen NA et al.
Neurobiology of Disease, 2024
Unravelling the Genetic Landscape of Hemiplegic Migraine: Exploring Innovative Strategies and Emerging Approaches.
Alfayyadh MM et al.
Genes, 2024
The Na/K-ATPase α1/Src Signaling Axis Regulates Mitochondrial Metabolic Function and Redox Signaling in Human iPSC-Derived Cardiomyocytes.
Cai L et al.
Biomedicines, 2023
Genetic Mechanisms of Migraine: Insights from Monogenic Migraine Mutations.
Gosalia H et al.
International Journal of Molecular Sciences, 2023
Hypercontractile Cardiac Phenotype in Mice with Migraine-Associated Mutation in the Na+,K+-ATPase α2-Isoform.
Rajanathan R et al.
Cells, 2023
Astrocytic Glutamate Transporters and Migraine.
Conti F et al.
Neurochemical Research, 2023
Pathophysiology of migraine aura.
Sanchez Del Rio M et al.
Handbook of Clinical Neurology, 2023
Genetics of migraine: Delineation of contemporary understanding of the genetic underpinning of migraine.
de Boer I et al.
Handbook of Clinical Neurology, 2023
Migraine-Associated Mutation in the Na,K-ATPase Leads to Disturbances in Cardiac Metabolism and Reduced Cardiac Function.
Staehr C et al.
Journal of the American Heart Association, 2022
Hyperexcitable interneurons trigger cortical spreading depression in an Scn1a migraine model.
Auffenberg E et al.
The Journal of Clinical Investigation, 2021
Functional correlation of ATP1A2 mutations with phenotypic spectrum: from pure hemiplegic migraine to its variant forms.
Li Y et al.
The Journal of Headache and Pain, 2021
Astrocyte deletion of α2-Na/K ATPase triggers episodic motor paralysis in mice via a metabolic pathway.
Smith SE et al.
Nature Communications, 2020
Abnormal neurovascular coupling as a cause of excess cerebral vasodilation in familial migraine.
Staehr C et al.
Cardiovascular Research, 2020
Characteristics of cortical spreading depression and c-Fos expression in transgenic mice having a mutation associated with familial hemiplegic migraine 2.
Tang C et al.
Cephalalgia : an International Journal of Headache, 2020
Genetics of migraine aura: an update.
de Boer I et al.
The Journal of Headache and Pain, 2020
Cell biology and dynamics of Neuronal Na+/K+-ATPase in health and diseases.
Shrivastava AN et al.
Neuropharmacology, 2020
Na+/K+-ATPase α isoform deficiency results in distinct spreading depolarization phenotypes.
Reiffurth C et al.
Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 2020
A Chinese family with familial hemiplegic migraine type 2 due to a novel missense mutation in ATP1A2.
Tang W et al.
Cephalalgia : an International Journal of Headache, 2019
Smooth muscle Ca2+ sensitization causes hypercontractility of middle cerebral arteries in mice bearing the familial hemiplegic migraine type 2 associated mutation.
Staehr C et al.
Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 2019
Genetic mouse models of migraine.
Pietrobon D et al.
The Journal of Headache and Pain, 2019
Increased susceptibility to cortical spreading depression and epileptiform activity in a mouse model for FHM2.
Kros L et al.
Scientific Reports, 2018
The α2β2 isoform combination dominates the astrocytic Na+ /K+ -ATPase activity and is rendered nonfunctional by the α2.G301R familial hemiplegic migraine type 2-associated mutation.
Stoica A et al.
Glia, 2017
ExACtly zero or once: A clinically helpful guide to assessing genetic variants in mild epilepsies.
Bennett CA et al.
Neurology. Genetics, 2017
Recurrent coma and fever in familial hemiplegic migraine type 2. A prospective 15-year follow-up of a large family with a novel ATP1A2 mutation.
Pelzer N et al.
Cephalalgia : an International Journal of Headache, 2017
Genetic insights into migraine and glutamate: a protagonist driving the headache.
Gasparini CF et al.
Journal of the Neurological Sciences, 2016
Glutamate-system defects behind psychiatric manifestations in a familial hemiplegic migraine type 2 disease-mutation mouse model.
Bøttger P et al.
Scientific Reports, 2016
Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.
Isaksen TJ et al.
Frontiers in Physiology, 2016
The Revolution in Migraine Genetics: From Aching Channels Disorders to a Next-Generation Medicine.
Pellacani S et al.
Frontiers in Cellular Neuroscience, 2016
ATP1A2 Mutations in Migraine: Seeing through the Facets of an Ion Pump onto the Neurobiology of Disease.
Friedrich T et al.
Frontiers in Physiology, 2016
Familial Hemiplegic Migraine with Severe Attacks: A New Report with ATP1A2 Mutation.
Martínez E et al.
Case Reports in Neurological Medicine, 2016
Neurovascular changes in prolonged migraine aura in FHM with a novel ATP1A2 gene mutation.
Iizuka T et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2012
Migraine- and dystonia-related disease-mutations of Na+/K+-ATPases: relevance of behavioral studies in mice to disease symptoms and neurological manifestations in humans.
Bøttger P et al.
Neuroscience and Biobehavioral Reviews, 2012
Hemiplegic migraine, seizures, progressive spastic paraparesis, mood disorder, and coma in siblings with low systemic serotonin.
Horvath GA et al.
Cephalalgia : an International Journal of Headache, 2011
A new Italian FHM2 family: clinical aspects and functional analysis of the disease-associated mutation.
Santoro L et al.
Cephalalgia : an International Journal of Headache, 2011
Early seizures and cerebral oedema after trivial head trauma associated with the CACNA1A S218L mutation.
Stam AH et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2009
Novel mutations affecting the Na, K ATPase alpha model complex neurological diseases and implicate the sodium pump in increased longevity.
Ashmore LJ et al.
Human Genetics, 2009
The structure of the Na+,K+-ATPase and mapping of isoform differences and disease-related mutations.
Morth JP et al.
Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 2009
Intravenous nimodipine worsening prolonged attack of familial hemiplegic migraine.
Mjåset C et al.
The Journal of Headache and Pain, 2008
The primary headaches: genetics, epigenetics and a behavioural genetic model.
Montagna P
The Journal of Headache and Pain, 2008
Two novel functional mutations in the Na+,K+-ATPase alpha2-subunit ATP1A2 gene in patients with familial hemiplegic migraine and associated neurological phenotypes.
Castro MJ et al.
Clinical Genetics, 2008