Endothelin Receptor A –231 G&gt;A Polymorphism: No Linkage to Primary Pediatric Headache

Lisi, Veronica; Garbo, Greta M.; Battistella, PierAntonio; Miccichè, Flavia; Stecca, Anna; Terrazzino, Salvatore; Franzoi, Malida; Tripoli, E; Leon, A. S.; Clementi, Maurizio

doi:10.1111/j.1526-4610.2006.00380.x

Cited by 15 publications

(16 citation statements)

References 13 publications

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“…Interestingly, the potent vasoconstrictor endothelin (ET) 1, whose effect is mediated via ET type A and B receptors, has been shown as a potent inducer of CSD [Dreier et al, 2002]. However further studies have been undertaken in a pediatric Italian cohort investigating the same polymorphism, and failed to replicate the earlier positive association [Lisi et al, 2006].…”

Section: Vascular Genesmentioning

confidence: 99%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

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Migraine is a common complex neurological disorder with a well-known but poorly characterized genetic liability. The search for migraine susceptibility genes has been the focus of intense research. It is now believed that common migraine is not a single gene disorder, but attributable to several potentially interacting genetic variants. These variants may differ in each sufferer and interact with environmental factors to set the individual migraine threshold. This genetic liability may play an important role in the clinical heterogeneity seen in migraine and also in the variability of treatment response. This review will look at genetic loci implicated in migraine to date and consider their current or prospective role in migraine therapy. To elucidate the complex nature of migraine genetic liability, approaches that consider detailed endophenotypic profiles that encompass treatment response may provide much more relevant information than simple end diagnosis. Drug Dev Res 68: 282-293, 2007. r 2007 Wiley-Liss, Inc.

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Section: Vascular Genesmentioning

confidence: 99%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

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“…Our experience Given the increased familial risk in relatives of migraine probands, we have, among the genes shown to be associated to adult migraine liability, recently focused on whether the -231 G>A polymorphism in the endothelin 1 type A receptor (EDNRA) shown to strongly modulate the risk of adult migraine [13] contributes to paediatric migraine susceptibility. Results to date obtained, however, show that the -231 G>A polymorphism in the EDNRA gene is neither associated with primary juvenile headache nor significantly correlated with main clinical features characteristic of the headache pathology, thus suggesting the possibility of an age-related interaction of the EDNRA polymorphic variant on migraine liability and disease expression [14].…”

Section: Molecular Studies Of the Genetic Factors In Adult Migrainementioning

confidence: 79%

Genetic risk factors in primary paediatric versus adult headache: complexities and problematics

et al. 2005

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IntroductionRecurring primary headaches, such as migraine or tension-type, are common during childhood (2.5%) and adolescence (15%) [1]. However, while ever increasing evidence shows that migraine is a complex neurovascular disorder with genetic factors playing a primary role in its aetiology, none of the genetic factors which have to date been shown to be linked to adult migraine susceptibility have been investigated in children, for whom primary headaches represent frequent causes for referral for neurologic assessment. In addition, while epidemiological, twin and family studies have revealed that approximately one-half of its variation is attributable to additive genes, with a negligible contribution of nonadditive genetic effects [2], the identification and validation of the underlying genetic risk factors poses enormous challenges even in adult migraine. The severity of migraine symptoms, such as the recurrence and duration of attacks and the age of onset, are variable among patients, thus rendering difficult both the definition of the appropriate phenotype as J Headache Pain (2005) Genetic polymorphisms have been evaluated in association studies, some of which have been suggested to be susceptibility markers for adult migraine. To date, however, none of the identified polymorphisms in adult migraine susceptibility have been investigated in children, raising the possibility that they may not be necessarily involved in paediatric migraine susceptibility. This paper reviews studies of the genetic basis of migraine and summarises our experience in genetic association studies in primary paediatric headache susceptibility.6:179-181 DOI 10.1007/s10194-005-0178-x Genetic risk factors in primary paediatric versus adult headache: complexities and problematics G E N E

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“…Goadsby and colleagues [1996] have also reported that ET does not play a significant role in the vasoconstrictor portion of the cerebral blood flow change seen in the spreading depression, nor does it affect the resting flow in an in vitro model using the middle cerebral artery, harvested from cats postmortem. Also in this respect, the ET A (-231 A/G) polymorphism, which was reported to be associated with migraine [Tzourio et al, 2001], was subsequently found to be neither associated with primary juvenile headache nor correlated with main clinical features characteristic of the headache pathology in pediatric settings [Lisi et al, 2006].…”

Section: Cgrp Sp and Nka Involvement In Migrainementioning

confidence: 96%

Role of neuropeptides in migraine: where do they stand in the latest expert recommendations in migraine treatment?

Samsam

Coveñas

Ahangari

et al. 2007

Drug Development Research

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Many factors have been implicated in the pathogenesis of migraine headache, including activation of the trigeminovascular system, dysfunction of: cerebral blood vessels, circulating vasoactive substances, mitochondrial energy metabolism, brain oxygenation and metabolism, platelet disorder, alterations in serotonin levels, low levels of brain tissue magnesium, altered transport of ions across the cell membrane, and inheritance and dysfunction of the brainstem periaqueductal gray matter. The headache phase of migraine is associated with cerebral vasodilation and inflammation, presumably mediated by the release of vasoactive substances and neuropeptides including CGRP (calcitonin gene-related peptide). Increased serum CGRP levels have been detected during migraine and cluster headache. One strategy to treat migraine is to inhibit the release of neuropeptides or to block their receptors. This article briefly reviews some experimental and clinical investigations focused on neuropeptide involvement in migraine. Drug Dev Res 68: 294-314, 2007.

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Endothelin Receptor A –231 G>A Polymorphism: No Linkage to Primary Pediatric Headache

Abstract: Our study shows that the -231 G>A polymorphism in the EDNRA gene is neither associated with primary juvenile headache nor significantly correlated with main clinical features characteristic of the headache pathology in pediatric settings.

Cited by 15 publications

References 13 publications

Migraine genetics and prospects for pharmacotherapy

Migraine genetics and prospects for pharmacotherapy

Genetic risk factors in primary paediatric versus adult headache: complexities and problematics

Role of neuropeptides in migraine: where do they stand in the latest expert recommendations in migraine treatment?

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