Nutrient Effects on Motor Neurons and the Risk of Amyotrophic Lateral Sclerosis

Abstract

Amyotrophic lateral sclerosis (ALS) is an incurable chronic progressive neurodegenerative disease with the progressive degeneration of motor neurons in the motor cortex and lower motor neurons in the spinal cord and the brain stem. The etiology and pathogenesis of ALS are being actively studied, but there is still no single concept. The study of ALS risk factors can help to understand the mechanism of this disease development and, possibly, slow down the rate of its progression in patients and also reduce the risk of its development in people with a predisposition toward familial ALS. The interest of researchers and clinicians in the protective role of nutrients in the development of ALS has been increasing in recent years. However, the role of some of them is not well-understood or disputed. The objective of this review is to analyze studies on the role of nutrients as environmental factors affecting the risk of developing ALS and the rate of motor neuron degeneration progression. Methods: We searched the PubMed, Springer, Clinical keys, Google Scholar, and E-Library databases for publications using keywords and their combinations. We analyzed all the available studies published in 2010–2020. Discussion: We analyzed 39 studies, including randomized clinical trials, clinical cases, and meta-analyses, involving ALS patients and studies on animal models of ALS. This review demonstrated that the following vitamins are the most significant protectors of ALS development: vitamin B12, vitamin E > vitamin C > vitamin B1, vitamin B9 > vitamin D > vitamin B2, vitamin B6 > vitamin A, and vitamin B7. In addition, this review indicates that the role of foods with a high content of cholesterol, polyunsaturated fatty acids, urates, and purines plays a big part in ALS development. Conclusion: The inclusion of vitamins and a ketogenic diet in disease-modifying ALS therapy can reduce the progression rate of motor neuron degeneration and slow the rate of disease progression, but the approach to nutrient selection must be personalized. The roles of vitamins C, D, and B7 as ALS protectors need further study.

Dietary-Derived Essential Nutrients and Amyotrophic Lateral Sclerosis: A Two-Sample Mendelian Randomization Study

“…Vitamin E is another common essential vitamin [ 72 ], which mainly provides antioxidative protection against lipid peroxidation, reactive oxygen species (ROS), and reactive nitrogen species (RNS) [ 73 ]. The results of several large prospective cohort studies implied that the regular use of vitamin E supplements has a time-dependent protective effect on ALS [ 10 , 74 ].…”

Prospects for studying the pharmacokinetics, pharmacodynamics and pharmacogenetics of vitamin C in patients with neurological diseases and mental disorders

“…Careful choice of the dose and regimen of vitamin C intake is necessary for patients with an unfavorable pharmacogenetic profile, in particular in carriers of SNVs candidate genes encoding ascorbate and DHA transporter proteins through the blood-brain barrier, the membrane of neurons and the membrane of renal tubule cells. Despite numerous studies on the important role of vitamin C in the development and function of the central nervous system and PNS [72], the role of ascorbate pharmacogenetics has not been sufficiently studied. This is the reason for local and large interregional associative genetic studies of vitamin C pharmacogenetics in various ethnic groups and climatageographic regions in patients with neurological and mental disorders having different dietary habits.…”

P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis

“…Dysfunction in the pyruvate dehydrogenase enzyme and/or in its metabolic modulators (i.e., kinases and phosphatases) would prevent the passage of glycolysis into the Krebs cycle [55,56,57]. A family history of diabetes and/or epilepsy also suggests defects in this enzyme and is correlated with ALS disease (studies of confidential medical reports were obtained from clinical trials and references [58,59,60,61, 62]).…”