A study of oxidative stress in migraine with special reference to prophylactic therapy

Tripathi, Gyanesh M.; Kalita, Jayantee; Misra, U. K.

doi:10.1080/00207454.2017.1374959

Cited by 52 publications

(64 citation statements)

References 34 publications

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“…This link is supported by studies in which markers of increased oxi dative or nitrosative stress and/or decreased antioxidant capacity have been directly examined [54][55][56][57][58][59][60][61][62][63][64][65][66][67] (Supplementary Table 2). All studies of oxidative stress and/or antioxidant capacity in migraine have demonstrated that at least one marker is abnormal [54][55][56][57][58][59][60][61][62][63][64][65][66][67] . Of all biomarkers examined, superoxide dismutase activity seems to be the only one that is consistently reduced in patients with migraine, including interictally 68 .…”

Section: Oxidative and Nitrosative Stress And Antioxidant Capacitymentioning

confidence: 93%

“…Other drugs used for prevention of migraine treat ment have clear metabolic effects. Amitriptyline also reduces markers of oxidative stress and increases anti oxidant capacity 65 . Valproate attenuates nitroglycerin induced trigeminovascular activation by preserving mitochondrial function in a rat model of migraine 211 and increases mitochondrial biogenesis 212 .…”

Section: Prophylactic Pharmaceuticalsmentioning

confidence: 99%

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The metabolic face of migraine — from pathophysiology to treatment

et al. 2019

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Migraine can be regarded as a conserved, adaptive response that occurs in genetically predisposed individuals with a mismatch between the brain's energy reserve and workload. Given the high prevalence of migraine, genotypes associated with the condition seem likely to have conferred an evolutionary advantage. Technological advances have enabled the examination of different aspects of cerebral metabolism in patients with migraine, and complementary animal research has highlighted possible metabolic mechanisms in migraine pathophysiology. An increasing amount of evidence-much of it clinical-suggests that migraine is a response to cerebral energy deficiency or oxidative stress levels that exceed antioxidant capacity and that the attack itself helps to restore brain energy homeostasis and reduces harmful oxidative stress levels. Greater understanding of metabolism in migraine offers novel therapeutic opportunities. In this Review , we describe the evidence for abnormalities in energy metabolism and mitochondrial function in migraine, with a focus on clinical data (including neuroimaging, biochemical, genetic and therapeutic studies), and consider the relationship of these abnormalities with the abnormal sensory processing and cerebral hyper-responsivity observed in migraine. We discuss experimental data to consider potential mechanisms by which metabolic abnormalities could generate attacks. Finally , we highlight potential treatments that target cerebral metabolism, such as nutraceuticals, ketone bodies and dietary interventions.

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Section: Oxidative and Nitrosative Stress And Antioxidant Capacitymentioning

confidence: 93%

Section: Prophylactic Pharmaceuticalsmentioning

confidence: 99%

The metabolic face of migraine — from pathophysiology to treatment

et al. 2019

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“…40 In non-mitochondrial migraine patients increased oxidative stress markers like malondialdehyde, total antioxidant activity, GSH/GSSG concentrations were observed as were decreased concentrations of plasma GSH, glutathionine-S-transferase (GST), and total antioxidant capacity compared to controls. 40,80 PET imaging with 56 Cu-ATSM and 18 FDG demonstrated increased oxidative stress and increased glucose metabolism following hyperemia in a MELAS syndrome patient with stroke-like episodes. 41 Importantly, to our best knowledge, so far none of these imaging studies have been done in migraine m.3243A>G patients without stroke-like episodes.…”

Section: Mitochondria: Structure Function and Pathologymentioning

confidence: 94%

Mitochondrial Migraine: Disentangling the angiopathy paradigm in m.3243A>G patients

Smeitink¹,

Koene²,

Saris³

et al. 2019

JIMD Reports

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Migraine, characterized by recurrent attacks of predominantly unilateral throbbing headache, affects approximately 15% of the adult population and is an important cause of disability worldwide. Knowledge required for the development of new classes of antimigraine drugs might come from studying rare metabolic diseases associated with migraine. An illustrative example of a monogenetic disorder associated with migraine is the spectrum of disorders caused by the m.3243A>G mutation in the mitochondrial transfer RNA Leucine. Reported migraine prevalence figures in patients with this particular mutation vary considerably, but compared to the general population, m.3243A>G patients have a higher migraine prevalence. This burdensome symptom might sometimes even be the only clinical feature in maternal relatives carrying the m.3243A>G mutation. Although the exact sequence of events and the relative importance of factors underlying migraine in m.3243A>G MELAS spectrum disorders are still enigmatic, substantial evidence in man exist that dysfunctional mitochondria in both the vascular, the smooth muscle cells and the neuronal system and the interaction between these are at the starting point of the migraine developing pathophysiological cascade. Exclusively based on results of studies performed in patients harboring the m.3243A>G mutation, either in vivo or ex vivo, we here summarize our current understanding of mitochondrial angiopathy associated migraine in m.3243A>G patients which knowledge might lead to potential new avenues for migraine drug development.

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“…Some studies have suggested that migraine may be the result of mitochondrial impairment, and therefore, since CoQ10 has been shown to improve mitochondrial oxidative phosphorylation in humans, it could be used as a successful migraine preventive to reduce the severity, length, and frequency of headaches (Rozen et al., ). In addition, there is an evidence of oxidative stress in migraine pathophysiology, which could explain the depletion of antioxidant levels in migraine patients when compared to controls (Tripathi, Kalita, & Misra, ). In fact, migraine patients have lower CoQ10 concentrations (Mason, ).…”

Section: Coq10 Supplementationmentioning

confidence: 99%

Coenzyme Q10 supplementation: Efficacy, safety, and formulation challenges

Arenas-Jal

Suñé-Negre

García-Montoya

2020

Comp Rev Food Sci Food Safe

123

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World population growth and aging are posing unprecedented challenges in sustaining the health of 9.1 billion people that will be occupying the planet by 2050. Although noncommunicable diseases such as cardiovascular and neurodegenerative diseases, cancer, and diabetes are among the top 10 global causes of death, they can be prevented by risk factor reduction, early detection, and adequate treatment. Since a healthy diet along with dietary supplementation could play an important role to reduce morbidity and cut off its associated health care costs, research in the food and nutrition area is required to find solutions to global challenges affecting health. As a result of the healthy living trend, dietary supplements category is growing fast, leading to an urgent need for dietitians, physicians, and policy makers to broaden the scientific evidence on the efficacy and safety of a wide range of active ingredients. Coenzyme Q10 (CoQ10), as the third most consumed dietary supplement, and as a potential candidate for the treatment of various noncommunicable diseases that are among the global top 10 causes of death, has gained interest over years. Scientific evidence regarding mainly CoQ10 efficacy and safety, as well as formulation challenges, is addressed in this review.

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A study of oxidative stress in migraine with special reference to prophylactic therapy

Abstract: There is evidence of oxidative stress in migraine pathophysiology. Following treatment, oxidative stress declined following both pharmacological and rTMS.

Cited by 52 publications

References 34 publications

The metabolic face of migraine — from pathophysiology to treatment

The metabolic face of migraine — from pathophysiology to treatment

Mitochondrial Migraine: Disentangling the angiopathy paradigm in m.3243A>G patients

Coenzyme Q10 supplementation: Efficacy, safety, and formulation challenges

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