Riboflavin Has Neuroprotective Potential: Focus on Parkinson's Disease and Migraine

被引:81
作者
Marashly, Eyad T. [1 ]
Bohlega, Saeed A. [1 ]
机构
[1] King Faisal Specialist Hosp & Res Ctr, Dept Neurosci, Riyadh, Saudi Arabia
关键词
riboflavin; Parkinson's disease; migraine; oxidative stress; glutamate excitotoxicity; pyridoxal phosphate; homocysteine; kynurenine; COMPLEX-I DEFICIENCY; NF-KAPPA-B; TRIGEMINAL NUCLEUS CAUDALIS; RED MEAT PROMOTE; OXIDATIVE STRESS; MTHFR C677T; NEURODEGENERATIVE DISORDERS; MITOCHONDRIAL BIOGENESIS; INFLAMMATORY CYTOKINES; SENSITIZED DEGRADATION;
D O I
10.3389/fneur.2017.00333
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
With the huge negative impact of neurological disorders on patient's life and society resources, the discovery of neuroprotective agents is critical and cost-effective. Neuroprotective agents can prevent and/or modify the course of neurological disorders. Despite being underestimated, riboflavin offers neuroprotective mechanisms. Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson's disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future.
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页数:12
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共 101 条
[1]   DEPENDENCE OF PYRIDOXINE METABOLISM ON RIBOFLAVIN STATUS IN SICKLE-CELL PATIENTS [J].
ADELEKAN, DA ;
ADEKILE, AD ;
THURNHAM, DI .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1987, 46 (01) :86-90
[2]  
Alp R, 2010, EUR REV MED PHARMACO, V14, P877
[3]   A further update on the role of excitotoxicity in the pathogenesis of Parkinson's disease [J].
Ambrosi, Giulia ;
Cerri, Silvia ;
Blandini, Fabio .
JOURNAL OF NEURAL TRANSMISSION, 2014, 121 (08) :849-859
[4]   Riboflavin (vitamin B2) and oxidative stress: a review [J].
Ashoori, Marziyeh ;
Saedisomeolia, Ahmad .
BRITISH JOURNAL OF NUTRITION, 2014, 111 (11) :1985-1991
[5]   Treatment of Mitochondrial Disorders [J].
Avula, Sreenivas ;
Parikh, Sumit ;
Demarest, Scott ;
Kurz, Jonathan ;
Gropman, Andrea .
CURRENT TREATMENT OPTIONS IN NEUROLOGY, 2014, 16 (06)
[6]   The TRPA1 channel in migraine mechanism and treatment [J].
Benemei, S. ;
Fusi, C. ;
Trevisan, Gabriela ;
Geppetti, Pierangelo .
BRITISH JOURNAL OF PHARMACOLOGY, 2014, 171 (10) :2552-2567
[7]   TREATMENT OF COMPLEX-I DEFICIENCY WITH RIBOFLAVIN [J].
BERNSEN, PLJA ;
GABREELS, FJM ;
RUITENBEEK, W ;
HAMBURGER, HL .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1993, 118 (02) :181-187
[8]  
Blandini F, 2010, FUNCT NEUROL, V25, P65
[9]   Oxidative stress and Parkinson's disease [J].
Blesa, Javier ;
Trigo-Damas, Ines ;
Quiroga-Varela, Anna ;
Jackson-Lewis, Vernice R. .
FRONTIERS IN NEUROANATOMY, 2015, 9
[10]   Vitamin D3 alters microglia immune activation by an IL-10 dependent SOCS3 mechanism [J].
Boontanrart, Mandy ;
Hall, Samuel D. ;
Spanier, Justin A. ;
Hayes, Colleen E. ;
Olson, Julie K. .
JOURNAL OF NEUROIMMUNOLOGY, 2016, 292 :126-136