Headache Group, NIHR King's Clinical Research Facility and SLaM Biomedical Research Centre, The Wolfson Sensory, Pain and Regeneration Research Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 9PJ, UK.
Department of Neurology, University of California, Los Angeles, CA 90095, USA.
Int J Mol Sci. 2023 Jul 26;24(15):11993. doi: 10.3390/ijms241511993.
Migraine is a common condition with disabling attacks that burdens people in the prime of their working lives. Despite years of research into migraine pathophysiology and therapeutics, much remains to be learned about the mechanisms at play in this complex neurovascular condition. Additionally, there remains a relative paucity of specific and targeted therapies available. Many sufferers remain underserved by currently available broad action preventive strategies, which are also complicated by poor tolerance and adverse effects. The development of preclinical migraine models in the laboratory, and the advances in human experimental migraine provocation, have led to the identification of key molecules likely involved in the molecular circuity of migraine, and have provided novel therapeutic targets. Importantly, the identification that vasoconstriction is neither necessary nor required for headache abortion has changed the landscape of migraine treatment and has broadened the therapy targets for patients with vascular risk factors or vascular disease. These targets include nitric oxide synthase (NOS) and several neuropeptides that are involved in migraine. The ability of NO donors and infusion of some of these peptides into humans to trigger typical migraine-like attacks has supported the development of targeted therapies against these molecules. Some of these, such as those targeting calcitonin gene-related peptide (CGRP), have already reached clinical practice and are displaying a positive outcome in migraineurs for the better by offering targeted efficacy without significant adverse effects. Others, such as those targeting pituitary adenylate cyclase activating polypeptide (PACAP), are showing promise and are likely to enter phase 3 clinical trials in the near future. Understanding these nitrergic and peptidergic mechanisms in migraine and their interactions is likely to lead to further therapeutic strategies for migraine in the future.
偏头痛是一种常见的致残性疾病,在人们工作的黄金时期给他们带来了负担。尽管多年来对偏头痛的病理生理学和治疗学进行了研究,但对于这种复杂的神经血管疾病中起作用的机制仍有许多需要了解。此外,可用的特异性和靶向治疗方法仍然相对较少。许多患者仍然无法从目前可用的广泛作用预防性策略中受益,这些策略还因耐受性差和不良反应而变得复杂。实验室中偏头痛前临床模型的发展,以及人类实验性偏头痛诱发的进展,导致了鉴定可能参与偏头痛分子回路的关键分子,并提供了新的治疗靶点。重要的是,血管收缩对于头痛缓解既不是必需的也不是必需的,这改变了偏头痛治疗的格局,并拓宽了具有血管危险因素或血管疾病的患者的治疗靶点。这些靶点包括一氧化氮合酶(NOS)和几种参与偏头痛的神经肽。NO 供体的能力和一些这些肽类在人类中输注可以引发典型的偏头痛样发作,这支持了针对这些分子的靶向治疗的发展。其中一些,如针对降钙素基因相关肽(CGRP)的靶向治疗,已经进入临床实践,并通过提供靶向疗效而没有明显的不良反应,为偏头痛患者带来了更好的效果。其他一些,如针对垂体腺苷酸环化酶激活肽(PACAP)的靶向治疗,显示出希望,并可能在不久的将来进入 3 期临床试验。了解偏头痛中的这些氮能和肽能机制及其相互作用,可能会为未来偏头痛的治疗提供进一步的治疗策略。