Literature DB >> 28380698

Myoclonus epilepsy and ataxia due to KCNC1 mutation: Analysis of 20 cases and K+ channel properties.

Karen L Oliver1, Silvana Franceschetti2, Carol J Milligan3, Mikko Muona4,5,6,7, Simone A Mandelstam8,9,10, Laura Canafoglia2, Anna M Boguszewska-Chachulska11, Amos D Korczyn12, Francesca Bisulli13,14, Carlo Di Bonaventura15, Francesca Ragona16, Roberto Michelucci13,17, Bruria Ben-Zeev12,18, Rachel Straussberg12,19, Ferruccio Panzica2, João Massano20,21, Daniel Friedman22, Arielle Crespel23, Bernt A Engelsen24, Frederick Andermann25,26, Eva Andermann27,28, Krystyna Spodar11, Anetta Lasek-Bal29, Patrizia Riguzzi13,17, Elena Pasini13,17, Paolo Tinuper13,14, Laura Licchetta13,14, Elena Gardella30,31, Matthias Lindenau32, Annette Wulf32, Rikke S Møller30,31, Felix Benninger33, Zaid Afawi12, Guido Rubboli13,34, Christopher A Reid3, Snezana Maljevic3,35, Holger Lerche35, Anna-Elina Lehesjoki5,6,7, Steven Petrou3,36, Samuel F Berkovic1.   

Abstract

OBJECTIVE: To comprehensively describe the new syndrome of myoclonus epilepsy and ataxia due to potassium channel mutation (MEAK), including cellular electrophysiological characterization of observed clinical improvement with fever.
METHODS: We analyzed clinical, electroclinical, and neuroimaging data for 20 patients with MEAK due to recurrent KCNC1 p.R320H mutation. In vitro electrophysiological studies were conducted using whole cell patch-clamp to explore biophysical properties of wild-type and mutant KV 3.1 channels.
RESULTS: Symptoms began at between 3 and 15 years of age (median = 9.5), with progressively severe myoclonus and rare tonic-clonic seizures. Ataxia was present early, but quickly became overshadowed by myoclonus; 10 patients were wheelchair-bound by their late teenage years. Mild cognitive decline occurred in half. Early death was not observed. Electroencephalogram (EEG) showed generalized spike and polyspike wave discharges, with documented photosensitivity in most. Polygraphic EEG-electromyographic studies demonstrated a cortical origin for myoclonus and striking coactivation of agonist and antagonist muscles. Magnetic resonance imaging revealed symmetrical cerebellar atrophy, which appeared progressive, and a prominent corpus callosum. Unexpectedly, transient clinical improvement with fever was noted in 6 patients. To explore this, we performed high-temperature in vitro recordings. At elevated temperatures, there was a robust leftward shift in activation of wild-type KV 3.1, increasing channel availability.
INTERPRETATION: MEAK has a relatively homogeneous presentation, resembling Unverricht-Lundborg disease, despite the genetic and biological basis being quite different. A remarkable improvement with fever may be explained by the temperature-dependent leftward shift in activation of wild-type KV 3.1 subunit-containing channels, which would counter the loss of function observed for mutant channels, highlighting KCNC1 as a potential target for precision therapeutics. Ann Neurol 2017;81:677-689.
© 2017 American Neurological Association.

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Year:  2017        PMID: 28380698     DOI: 10.1002/ana.24929

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  16 in total

1.  Progressive myoclonus epilepsies-Residual unsolved cases have marked genetic heterogeneity including dolichol-dependent protein glycosylation pathway genes.

Authors:  Carolina Courage; Karen L Oliver; Eon Joo Park; Jillian M Cameron; Kariona A Grabińska; Mikko Muona; Laura Canafoglia; Antonio Gambardella; Edith Said; Zaid Afawi; Betul Baykan; Christian Brandt; Carlo di Bonaventura; Hui Bein Chew; Chiara Criscuolo; Leanne M Dibbens; Barbara Castellotti; Patrizia Riguzzi; Angelo Labate; Alessandro Filla; Anna T Giallonardo; Geza Berecki; Christopher B Jackson; Tarja Joensuu; John A Damiano; Sara Kivity; Amos Korczyn; Aarno Palotie; Pasquale Striano; Davide Uccellini; Loretta Giuliano; Eva Andermann; Ingrid E Scheffer; Roberto Michelucci; Melanie Bahlo; Silvana Franceschetti; William C Sessa; Samuel F Berkovic; Anna-Elina Lehesjoki
Journal:  Am J Hum Genet       Date:  2021-04-01       Impact factor: 11.025

Review 2.  Ion Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies.

Authors:  Julia Oyrer; Snezana Maljevic; Ingrid E Scheffer; Samuel F Berkovic; Steven Petrou; Christopher A Reid
Journal:  Pharmacol Rev       Date:  2018-01       Impact factor: 25.468

3.  Cryo-EM structure of the human Kv3.1 channel reveals gating control by the cytoplasmic T1 domain.

Authors:  Gamma Chi; Qiansheng Liang; Akshay Sridhar; John B Cowgill; Kasim Sader; Mazdak Radjainia; Pu Qian; Pablo Castro-Hartmann; Shayla Venkaya; Nanki Kaur Singh; Gavin McKinley; Alejandra Fernandez-Cid; Shubhashish M M Mukhopadhyay; Nicola A Burgess-Brown; Lucie Delemotte; Manuel Covarrubias; Katharina L Dürr
Journal:  Nat Commun       Date:  2022-07-15       Impact factor: 17.694

4.  Timing is everything: structural insights into the disease-linked Kv3 channels controlling fast action-potential firing in the brain.

Authors:  Martin J Gunthorpe
Journal:  Nat Commun       Date:  2022-07-15       Impact factor: 17.694

5.  KCTD7 deficiency defines a distinct neurodegenerative disorder with a conserved autophagy-lysosome defect.

Authors:  Kyle A Metz; Xinchen Teng; Isabelle Coppens; Heather M Lamb; Bart E Wagner; Jill A Rosenfeld; Xianghui Chen; Yu Zhang; Hee Jong Kim; Michael E Meadow; Tim Sen Wang; Edda D Haberlandt; Glenn W Anderson; Esther Leshinsky-Silver; Weimin Bi; Thomas C Markello; Marsha Pratt; Nawal Makhseed; Adolfo Garnica; Noelle R Danylchuk; Thomas A Burrow; Parul Jayakar; Dianalee McKnight; Satish Agadi; Hatha Gbedawo; Christine Stanley; Michael Alber; Isabelle Prehl; Katrina Peariso; Min Tsui Ong; Santosh R Mordekar; Michael J Parker; Daniel Crooks; Pankaj B Agrawal; Gerard T Berry; Tobias Loddenkemper; Yaping Yang; Gustavo H B Maegawa; Abdel Aouacheria; Janet G Markle; James A Wohlschlegel; Adam L Hartman; J Marie Hardwick
Journal:  Ann Neurol       Date:  2018-11-08       Impact factor: 10.422

Review 6.  Myoclonus-Ataxia Syndromes: A Diagnostic Approach.

Authors:  Malco Rossi; Sterre van der Veen; Marcelo Merello; Marina A J Tijssen; Bart van de Warrenburg
Journal:  Mov Disord Clin Pract       Date:  2020-11-03

7.  KCNC1-related disorders: new de novo variants expand the phenotypic spectrum.

Authors:  Joohyun Park; Mahmoud Koko; Ulrike B S Hedrich; Andreas Hermann; Kirsten Cremer; Edda Haberlandt; Mona Grimmel; Bader Alhaddad; Stefanie Beck-Woedl; Merle Harrer; Daniela Karall; Lisa Kingelhoefer; Andreas Tzschach; Lars C Matthies; Tim M Strom; Erich Bernd Ringelstein; Marc Sturm; Hartmut Engels; Markus Wolff; Holger Lerche; Tobias B Haack
Journal:  Ann Clin Transl Neurol       Date:  2019-06-07       Impact factor: 4.511

8.  A Kinetic Map of the Homomeric Voltage-Gated Potassium Channel (Kv) Family.

Authors:  Rajnish Ranjan; Emmanuelle Logette; Michela Marani; Mirjia Herzog; Valérie Tâche; Enrico Scantamburlo; Valérie Buchillier; Henry Markram
Journal:  Front Cell Neurosci       Date:  2019-08-20       Impact factor: 5.505

9.  Encephalopathies with KCNC1 variants: genotype-phenotype-functional correlations.

Authors:  Jillian M Cameron; Snezana Maljevic; Umesh Nair; Ye Htet Aung; Benjamin Cogné; Stéphane Bézieau; Edward Blair; Bertrand Isidor; Christiane Zweier; André Reis; Mary Kay Koenig; Timothy Maarup; Dean Sarco; Alexandra Afenjar; A H M Mahbubul Huq; Mary Kukolich; Thierry Billette de Villemeur; Caroline Nava; Bénédicte Héron; Steven Petrou; Samuel F Berkovic
Journal:  Ann Clin Transl Neurol       Date:  2019-07-01       Impact factor: 4.511

10.  Deep Transcriptomic Analysis Reveals the Dynamic Developmental Progression during Early Development of Channel Catfish (Ictalurus punctatus).

Authors:  Xiaoli Ma; Baofeng Su; Yuan Tian; Nathan J C Backenstose; Zhi Ye; Anthony Moss; Thuy-Yen Duong; Xu Wang; Rex A Dunham
Journal:  Int J Mol Sci       Date:  2020-08-02       Impact factor: 5.923

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