Effectiveness of high‐dose riboflavin in migraine prophylaxis A randomized controlled trial

Schoenen, Jean; Jacquy, J; Lenaerts, Marc

doi:10.1212/wnl.50.2.466

Cited by 463 publications

(272 citation statements)

References 18 publications

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“…Menadione and ascorbate together can act as complex IV substrates and sustain mitochondrial ETC respiration when complex III is compromised [79]. Other compounds that enhance mitochondrial ETC and oxidative phosphorylation include nicotinamide, a precursor to the complex I substrate, nicotinamide adenine dinucleotide, and riboflavin, a precursor to the complex II substrate, flavin adenine dinucleotdie [84]. While outcomes of research on these molecules have shown promising potential in preclinical studies, their efficacy clinically is unlikely to be substantial as they target specific components of the bioenergetic system instead of the entire system.…”

Section: Mitochondrial Bioenergetics As a Therapeutic Targetmentioning

confidence: 99%

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

2015

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Alzheimer's disease (AD) has a complex and progressive neurodegenerative phenotype, with hypometabolism and impaired mitochondrial bioenergetics among the earliest pathogenic events. Bioenergetic deficits are well documented in preclinical models of mammalian aging and AD, emerge early in the prodromal phase of AD, and in those at risk for AD. This review discusses the importance of early therapeutic intervention during the prodromal stage that precedes irreversible degeneration in AD. Mechanisms of action for current mitochondrial and bioenergetic therapeutics for AD broadly fall into the following categories: 1) glucose metabolism and substrate supply; 2) mitochondrial enhancers to potentiate energy production; 3) antioxidants to scavenge reactive oxygen species and reduce oxidative damage; 4) candidates that target apoptotic and mitophagy pathways to either remove damaged mitochondria or prevent neuronal death. Thus far, mitochondrial therapeutic strategies have shown promise at the preclinical stage but have had little-to-no success in clinical trials. Lessons learned from preclinical and clinical therapeutic studies are discussed. Understanding the bioenergetic adaptations that occur during aging and AD led us to focus on a systems biology approach that targets the bioenergetic system rather than a single component of this system. Bioenergetic system-level therapeutics personalized to bioenergetic phenotype would target bioenergetic deficits across the prodromal and clinical stages to prevent and delay progression of AD.

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Section: Mitochondrial Bioenergetics As a Therapeutic Targetmentioning

confidence: 99%

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

2015

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“…ATP was found to be reduced in the occipital lobe of MwoA patients, however, ATP remains to be measured in MwA patients. Additional evidence supporting a disturbed energy metabolism in migraine, comes from pharmacological studies showing the effects of metabolic enhancers, such as riboflavin and coenzyme Q10 (both with a well defined role in mitochondrial membrane generation of ATP), in migraine prophylaxis (65)(66)(67)(68). It is worthy of note that the therapeutic response to riboflavin was associated with specific mitochondrial DNA haplogroups (69).…”

Section: Functional Paradigmmentioning

confidence: 99%

Magnetic resonance spectroscopy in migraine: What have we learned so far?

2012

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Objective: To summarize and evaluate proton (1H) and phosphorus (31P) magnetic resonance spectroscopy (MRS) findings in migraine. Methods: A thorough review of 1H and/or 31P-MRS studies in any form of migraine published up to September 2011. Results: Some findings were consistent in all studies, such as a lack of ictal/interictal brain pH change and a disturbed energy metabolism, the latter of which is reflected in a drop in phosphocreatine content, both in the resting brain and in muscle following exercise. In a recent interictal study ATP was found to be significantly decreased in the occipital lobe of migraine with aura patients, reinforcing the concept of a mitochondrial component to the migraine threshold, at least in a subgroup of patients. In several studies a correlation between the extent of the energy disturbance and the clinical phenotype severity was apparent. Less consistent but still congruent with a disturbed energy metabolism is an observed lactate increase in the occipital cortex of several migraine subtypes (MwA, migraine with prolonged aura). No increases in brain glutamate levels were found. Conclusion: The combined abnormalities found in MRS studies imply a mitochondrial component in migraine neurobiology. This could be due to a primary mitochondrial dysfunction or be secondary to, for example, alterations in brain excitability. The extent of variation in the data can be attributed to both the variable clinical inclusion criteria used and the variation in applied methodology. Therefore it is necessary to continue to optimize MRS methodology to gain further insights, especially concerning lactate and glutamate.

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“…Merck (rizatriptan) went for a quicker onset of action. In two RCTs rizatriptan had a quicker onset of action than sumatriptan [13,14], whereas this was not the case in one RCT published much later [25]. Almirall (almotriptan) probably went for superior efficacy and for less AEs.…”

Section: Understanding a Paper On Drug Trials In Migrainementioning

confidence: 99%

“…The whole process is complicated and is in most cases funded and controlled by the pharmaceutical industry. There are, however, exceptions to this general rule, for example a RCT on riboflavin for migraine prophylaxis [14], which was conceived and funded independently.…”

Section: How a Clinical Trial In Migraine Is Donementioning

confidence: 99%

Understanding clinical trials in migraine

Tfelt‐Hansen

2006

J Headache Pain

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The following points are covered in this review.(1) How a randomised clinical trial in migraine is performed. The whole process from idea to publication of an article is reviewed. (2) How to understand a paper on clinical trials in migraine. The aim of the study, design of study, efficacy measures and presentation of results are reviewed. The aim of the study is often stated vaguely and it is suggested to look at the power calculations in order to understand the aim of the study. The aims and the results of the trial programmes of the triptans are reviewed. Results of the study should be presented with 95%CI. (3) How to understand meta-analyses in migraine. Relationship between meta-analyses and head-to-head comparative trials is reviewed; and it is concluded that head-to-head comparisons remain the "golden standard" with metaanalyses as a useful supplement.

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Effectiveness of high‐dose riboflavin in migraine prophylaxis A randomized controlled trial

Cited by 463 publications

References 18 publications

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

Magnetic resonance spectroscopy in migraine: What have we learned so far?

Understanding clinical trials in migraine

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