scholarly journals Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Author(s):  
Katharina Eikermann-Haerter ◽  
Ergin Dileköz ◽  
Chiho Kudo ◽  
Sean I. Savitz ◽  
Christian Waeber ◽  
...  
2011 ◽  
Vol 31 (15) ◽  
pp. 5755-5763 ◽  
Author(s):  
K. Eikermann-Haerter ◽  
I. Yuzawa ◽  
T. Qin ◽  
Y. Wang ◽  
K. Baek ◽  
...  

2015 ◽  
Vol 263 ◽  
pp. 214-220 ◽  
Author(s):  
Reinald Shyti ◽  
Katharina Eikermann-Haerter ◽  
Sandra H. van Heiningen ◽  
Onno C. Meijer ◽  
Cenk Ayata ◽  
...  

2009 ◽  
Vol 66 (4) ◽  
pp. 564-568 ◽  
Author(s):  
Katharina Eikermann-Haerter ◽  
Michael J. Baum ◽  
Michel D. Ferrari ◽  
Arn M.J.M. van den Maagdenberg ◽  
Michael A. Moskowitz ◽  
...  

2021 ◽  
Vol 22 (5) ◽  
pp. 2688
Author(s):  
Marta Kowalska ◽  
Michał Prendecki ◽  
Thomas Piekut ◽  
Wojciech Kozubski ◽  
Jolanta Dorszewska

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the α1A subunit of the P/Q-type voltage-gated calcium channel.


2019 ◽  
Vol 9 (7) ◽  
pp. 172 ◽  
Author(s):  
Salvo Lombardo ◽  
Emanuela Mazzon ◽  
Maria Basile ◽  
Eugenio Cavalli ◽  
Placido Bramanti ◽  
...  

Migraine is a disorder characterized by attacks of monolateral headaches, often accompanied by nausea, vomiting, and photophobia. Around 30% of patients also report aura symptoms. The cause of the aura is believed to be related to the cortical spreading depression (CSD), a wave of neuronal and glial depolarization originating in the occipital cortex, followed by temporary neuronal silencing. During a migraine attack, increased expression of inflammatory mediators, along with a decrease in the expression of anti-inflammatory genes, have been observed. The aim of this study was to evaluate the expression of inflammatory genes, in particular that of IL-1 receptor antagonist (IL-1RN), following CSD in a mouse model of familial hemiplegic migraine type 1 (FHM-1). We show here that the expression of IL-1RN was upregulated after the CSD, suggesting a possible attempt to modulate the inflammatory response. This study allows researchers to better understand the development of the disease and aids in the search for new therapeutic strategies in migraine.


2021 ◽  
pp. 105424
Author(s):  
Anisa Dehghani ◽  
Thas Phisonkunkasem ◽  
Sinem Yilmaz Ozcan ◽  
Turgay Dalkara ◽  
Arn M.J.M. van den Maagdenberg ◽  
...  

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