Brain Energy Deficit as a Source of Oxidative Stress in Migraine: A Molecular Basis for Migraine Susceptibility

2021 ◽  
Author(s):  
Jonathan M. Borkum
Keyword(s):  
Oxidative Stress ◽  
Molecular Basis ◽  
Energy Deficit ◽  
Brain Energy

scholarly journals Nutrients to Improve Mitochondrial Function to Reduce Brain Energy Deficit and Oxidative Stress in Migraine

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4433
Author(s):  
Michal Fila ◽  
Cezary Chojnacki ◽  
Jan Chojnacki ◽  
Janusz Blasiak
Keyword(s):  
Oxidative Stress ◽  
Energy Production ◽  
Brain Mitochondria ◽  
Energy Deficit ◽  
Main Process ◽  
Mitochondrial Functions ◽  
History Of ◽  
Migraine Pathogenesis ◽  
Migraine Triggers ◽  
Brain Energy

The mechanisms of migraine pathogenesis are not completely clear, but 31P-nuclear magnetic resonance studies revealed brain energy deficit in migraineurs. As glycolysis is the main process of energy production in the brain, mitochondria may play an important role in migraine pathogenesis. Nutrition is an important aspect of migraine pathogenesis, as many migraineurs report food-related products as migraine triggers. Apart from approved anti-migraine drugs, many vitamins and supplements are considered in migraine prevention and therapy, but without strong supportive evidence. In this review, we summarize and update information about nutrients that may be important for mitochondrial functions, energy production, oxidative stress, and that are related to migraine. Additionally, we present a brief overview of caffeine and alcohol, as they are often reported to have ambiguous effects in migraineurs. The nutrients that can be considered to supplement the diet to prevent and/or ameliorate migraine are riboflavin, thiamine, magnesium ions, niacin, carnitine, coenzyme Q10, melatonin, lipoic acid, pyridoxine, folate, and cobalamin. They can supplement a normal, healthy diet, which should be adjusted to individual needs determined mainly by the physiological constitution of an organism. The intake of caffeine and alcohol should be fine-tuned to the history of their use, as withdrawal of these agents in regular users may become a migraine trigger.

CRYPTIC CAUSES AND MECHANISMS INVOLVED IN AGEING

INDIAN DRUGS ◽  
2013 ◽  
Vol 50 (01) ◽  
pp. 5-22
Author(s):  
K Challabotla ◽  
◽  
D Banji ◽  
O.J.F Banji ◽  
Chilipi K Reddy
Keyword(s):  
Oxidative Stress ◽  
Developing Countries ◽  
Molecular Basis ◽  
Metabolic Disorders ◽  
Natural Process ◽  
Biological Functions ◽  
Stress Theory ◽  
Biochemical Alterations ◽  
Organ Systems ◽  
The Brain

Ageing is a natural process characterized by progressive deterioration of biological functions. Ageing causes both morphological as well as biochemical alterations in various body organs leading to deterioration of health. Proteins, enzymes and neurotransmitters are affected, which in turn can result in dysregulation of various pathways. WHO has reported that by 2020, three quarters of all deaths in developing countries will be age-associated. Currently more than 300 theories exist to explain the phenomenon of ageing; amongst them the oxidative stress theory of ageing is most studied and accepted for the molecular basis of ageing. All these processes can progress at an unprecedented pace on contact with triggering factors, leading to the development of pathological ageing. The probability of developing neurodegenerative and metabolic disorders is relatively high under such circumstances. This review emphasizes the theories and mechanisms of ageing and an overview on the aspects of age associated biochemical changes and the implications on the brain, liver and various organ systems.

Molecular Basis of Diabetic Peripheral Neuropathy: Role of Oxidative Stress

2015 ◽  
Vol 3 (2) ◽  
pp. 123-124
Author(s):  
Nisha Rani Jamwal ◽  
◽  
Senthil P Kumar. ◽  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Molecular Basis

scholarly journals The Bad, the Good, and the Ugly about Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Marlene Jimenez-Del-Rio ◽  
Carlos Velez-Pardo
Keyword(s):  
Oxidative Stress ◽  
Intracellular Signaling ◽  
Molecular Basis ◽  
Mechanistic Explanation ◽  
Etiologic Factor ◽  
Significant Implication ◽  
Design Strategies ◽  
Pathologic Process ◽  
Intracellular Signaling Pathways ◽  
Cell Death Signaling

Alzheimer’s disease (AD), Parkinson’s disease (PD), and cancer (e.g., leukemia) are the most devastating disorders affecting millions of people worldwide. Except for some kind of cancers, no effective and/or definitive therapeutic treatment aimed to reduce or to retard the clinic and pathologic symptoms induced by AD and PD is presently available. Therefore, it is urgently needed to understand the molecular basis of these disorders. Since oxidative stress (OS) is an important etiologic factor of the pathologic process of AD, PD, and cancer, understanding how intracellular signaling pathways respond to OS will have a significant implication in the therapy of these diseases. Here, we propose a model of minimal completeness of cell death signaling induced by OS as a mechanistic explanation of neuronal and cancer cell demise. This mechanism might provide the basis for therapeutic design strategies. Finally, we will attempt to associate PD, cancer, and OS. This paper critically analyzes the evidence that support the “oxidative stress model” in neurodegeneration and cancer.

scholarly journals Impact of lgt mutation on lipoprotein biosynthesis and in vitro phenotypes of Streptococcus agalactiae

Microbiology ◽  
2009 ◽  
Vol 155 (5) ◽  
pp. 1451-1458 ◽  
Author(s):  
Beverley A. Bray ◽  
Iain C. Sutcliffe ◽  
Dean J. Harrington
Keyword(s):  
Oxidative Stress ◽  
Streptococcus Agalactiae ◽  
Molecular Basis ◽  
Cell Envelope ◽  
Host Cells ◽  
Human Endothelial Cells ◽  
Increased Sensitivity ◽  
Group B

Although Streptococcus agalactiae, the group B Streptococcus, is a leading cause of invasive neonatal disease worldwide the molecular basis of its virulence is still poorly understood. To investigate the role of lipoproteins in the physiology and interaction of this pathogen with host cells, we generated a mutant S. agalactiae strain (A909ΔLgt) deficient in the Lgt enzyme and thus unable to lipidate lipoprotein precursors (pro-lipoproteins). The loss of pro-lipoprotein lipidation did not affect the viability of S. agalactiae or its growth in several different media, including cation-depleted media. The processing of two well-characterized lipoproteins, but not a non-lipoprotein, was clearly shown to be aberrant in A909ΔLgt. The mutant strain was shown to be more sensitive to oxidative stress in vitro although the molecular basis of this increased sensitivity was not apparent. The inactivation of Lgt also resulted in changes to the bacterial cell envelope, as demonstrated by reduced retention of both the group B carbohydrate and the polysaccharide capsule and a statistically significant reduction (P=0.0079) in A909ΔLgt adherence to human endothelial cells of fetal origin. These data confirm that failure to process lipoproteins correctly has pleiotropic effects that may be of significance to S. agalactiae colonization and pathogenesis.

scholarly journals Molecular Basis of Accelerated Aging with Immune Dysfunction-Mediated Inflammation (Inflamm-Aging) in Patients with Systemic Sclerosis

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3402
Author(s):  
Chieh-Yu Shen ◽  
Cheng-Hsun Lu ◽  
Cheng-Han Wu ◽  
Ko-Jen Li ◽  
Yu-Min Kuo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systemic Sclerosis ◽  
Cellular Senescence ◽  
Cancer Incidence ◽  
Molecular Basis ◽  
Chromosome Instability ◽  
Vascular Endothelial Cell ◽  
Accelerated Aging ◽  
Immune Dysfunction ◽  
Tissue Fibrosis

Systemic sclerosis (SSc) is a chronic connective tissue disorder characterized by immune dysregulation, chronic inflammation, vascular endothelial cell dysfunction, and progressive tissue fibrosis of the skin and internal organs. Moreover, increased cancer incidence and accelerated aging are also found. The increased cancer incidence is believed to be a result of chromosome instability. Accelerated cellular senescence has been confirmed by the shortening of telomere length due to increased DNA breakage, abnormal DNA repair response, and telomerase deficiency mediated by enhanced oxidative/nitrative stresses. The immune dysfunctions of SSc patients are manifested by excessive production of proinflammatory cytokines IL-1, IL-6, IL-17, IFN-α, and TNF-α, which can elicit potent tissue inflammation followed by tissue fibrosis. Furthermore, a number of autoantibodies including anti-topoisomerase 1 (anti-TOPO-1), anti-centromere (ACA or anti-CENP-B), anti-RNA polymerase enzyme (anti-RNAP III), anti-ribonuclear proteins (anti-U1, U2, and U11/U12 RNP), anti-nucleolar antigens (anti-Th/T0, anti-NOR90, anti-Ku, anti-RuvBL1/2, and anti-PM/Scl), and anti-telomere-associated proteins were also found. Based on these data, inflamm-aging caused by immune dysfunction-mediated inflammation exists in patients with SSc. Hence, increased cellular senescence is elicited by the interactions among excessive oxidative stress, pro-inflammatory cytokines, and autoantibodies. In the present review, we will discuss in detail the molecular basis of chromosome instability, increased oxidative stress, and functional adaptation by deranged immunome, which are related to inflamm-aging in patients with SSc.

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