Novel strategies for the treatment of migraine attacks via the CGRP, serotonin, dopamine, PAC1, and NMDA receptors

J. Tajti, Anett Csáti, L. Vécsei

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Introduction: Migraine is a common, paroxysmal, and disabling primary headache with a high personal and socioeconomic impact. It involves QQ 16% of the general population. During the years, a number of hypotheses have been put forward concerning the exact pathomechanism, but the final solution is still undiscovered. Areas covered: Although the origin is enigmatic, parallel therapeutic efforts have been developed. Current attack therapy does not meet the expectations of the patients or the doctors. This article, based on a PubMed search, reviews the novel pharmacological possibilities that influence the peripheral and central sensitization involved in the disease. Expert opinion: In order to overcome the therapeutic insufficiency, a calcitonin gene-related peptide receptor antagonist without the side-effect of liver transaminase elevation is required. Another therapeutic option is to develop a neurally acting antimigraine agent, such as a serotonin-1F receptor agonist, with low adverse central nervous system events. Development of a potent dopamine receptor antagonist is necessary to diminish the premonitory symptoms of migraine. A further option is to decrease the headache intensity with a pituitary adenylate cyclase-activating polypeptide type 1 receptor blocker which can cross the blood-brain barrier. Finally, synthetic kynurenine analogues are required to block the pain transmission in the activated trigeminal system.

Original languageEnglish
Pages (from-to)1509-1520
Number of pages12
JournalExpert Opinion on Drug Metabolism and Toxicology
Volume10
Issue number11
DOIs
Publication statusPublished - Nov 1 2014

Fingerprint

Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I
Calcitonin Gene-Related Peptide Receptors
Kynurenine
Dopamine Antagonists
Serotonin Receptors
Dopamine Receptors
Neurology
Transaminases
N-Methyl-D-Aspartate Receptors
Migraine Disorders
Liver
Headache
Central Nervous System Sensitization
Serotonin Receptor Agonists
Expert Testimony
Therapeutics
Blood-Brain Barrier
PubMed
Central Nervous System
Pharmacology

Keywords

  • 5-hydroxytryptamine 1F receptor agonist
  • Calcitonin gene-related peptide receptor antagonists
  • Dopamine receptor antagonists
  • Migraine attack therapy
  • N-methyl-D-aspartate receptor inhibitors
  • Pituitary adenylate cyclase-activating polypeptide type 1 receptor

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Medicine(all)

Cite this

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abstract = "Introduction: Migraine is a common, paroxysmal, and disabling primary headache with a high personal and socioeconomic impact. It involves QQ 16{\%} of the general population. During the years, a number of hypotheses have been put forward concerning the exact pathomechanism, but the final solution is still undiscovered. Areas covered: Although the origin is enigmatic, parallel therapeutic efforts have been developed. Current attack therapy does not meet the expectations of the patients or the doctors. This article, based on a PubMed search, reviews the novel pharmacological possibilities that influence the peripheral and central sensitization involved in the disease. Expert opinion: In order to overcome the therapeutic insufficiency, a calcitonin gene-related peptide receptor antagonist without the side-effect of liver transaminase elevation is required. Another therapeutic option is to develop a neurally acting antimigraine agent, such as a serotonin-1F receptor agonist, with low adverse central nervous system events. Development of a potent dopamine receptor antagonist is necessary to diminish the premonitory symptoms of migraine. A further option is to decrease the headache intensity with a pituitary adenylate cyclase-activating polypeptide type 1 receptor blocker which can cross the blood-brain barrier. Finally, synthetic kynurenine analogues are required to block the pain transmission in the activated trigeminal system.",
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