L
Ligia A. Papale
Researcher at University of Wisconsin-Madison
Publications - 50
Citations - 1494
Ligia A. Papale is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: DNA methylation & Epilepsy. The author has an hindex of 20, co-authored 47 publications receiving 1280 citations. Previous affiliations of Ligia A. Papale include Emory University & Federal University of São Paulo.
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Journal ArticleDOI
Altered Function of the SCN1A Voltage-gated Sodium Channel Leads to γ-Aminobutyric Acid-ergic (GABAergic) Interneuron Abnormalities
Melinda S. Martin,Karoni Dutt,Ligia A. Papale,Ligia A. Papale,Céline Dubé,Stacey B. B. Dutton,Georgius de Haan,Anupama Shankar,Sergio Tufik,Miriam H. Meisler,Tallie Z. Baram,Alan L. Goldin,Andrew Escayg +12 more
TL;DR: Results suggest that this SCN1A mutation predominantly impairs sodium channel activity in interneurons, leading to decreased inhibition, which may be a common mechanism underlying clinically distinct SCN 1A-derived disorders.
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The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy.
TL;DR: It is demonstrated that genetic interactions can alter seizure severity and support the hypothesis that genetic modifiers contribute to the clinical variability observed in SMEI and GEFS+.
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Preferential inactivation of Scn1a in parvalbumin interneurons increases seizure susceptibility.
Stacey B. B. Dutton,Christopher D. Makinson,Ligia A. Papale,Anupama Shankar,Bindu Balakrishnan,Kazu Nakazawa,Andrew Escayg +6 more
TL;DR: Reduced interneuron Scn1a expression resulted in the generation of spontaneous seizures, providing direct evidence for an important role of PV interneurons in the pathogenesis of ScN1a-derived epilepsies.
Journal ArticleDOI
Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice
Ligia A. Papale,Barbara Beyer,Julie M. Jones,Lisa M. Sharkey,Sergio Tufik,Michael P. Epstein,Verity A. Letts,Miriam H. Meisler,Wayne N. Frankel,Andrew Escayg +9 more
TL;DR: The abnormal EEG patterns in heterozygous mutant mice and the influence of genetic background on SWD make SCN8A an attractive candidate gene for common human absence epilepsy, a genetically complex disorder.
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A BAC transgenic mouse model reveals neuron subtype-specific effects of a Generalized Epilepsy with Febrile Seizures Plus (GEFS+) mutation
Bin Tang,Karoni Dutt,Ligia A. Papale,Raffaella Rusconi,Anupama Shankar,Jessica Ezzell Hunter,Sergio Tufik,Frank H. Yu,William A. Catterall,Massimo Mantegazza,Alan L. Goldin,Andrew Escayg +11 more
TL;DR: It is demonstrated that the effects of SCN1A mutations are cell type-dependent and that the R1648H mutation specifically leads to a reduction in interneuron excitability.