Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal disease related to upper and lower motor neurons degeneration. Although the environmental and genetic causes of this disease are still unclear, some factors involved in ALS onset such as oxidative stress may be influenced by diet. A higher risk of ALS has been correlated with a high fat and glutamate intake and β-methylamino-L-alanine. On the contrary, a diet based on antioxidant and anti-inflammatory compounds, such as curcumin, creatine, coenzyme Q10, vitamin E, vitamin A, vitamin C, and phytochemicals could reduce the risk of ALS. However, data are controversial as there is a discrepancy among different studies due to a limited number of samples and the many variables that are involved. In addition, an improper diet could lead to an altered microbiota and consequently to an altered metabolism that could predispose to the ALS onset. In this review we summarized some research that involve aspects related to ALS such as the epidemiology, the diet, the eating behaviour, the microbiota, and the metabolic diseases. Further research is needed to better comprehend the role of diet and the metabolic diseases in the mechanisms leading to ALS onset and progression.

Highlights

  • IntroductionAcademic Editors: Isabel Borrás and Jesús Lozano-Sánchez

  • The central role of food in daily life is known, more attention has to be paid to this aspect, especially in the medical field

  • The environmental and genetic causes that lead to the onset of Amyotrophic lateral sclerosis (ALS) are numerous and still to be clarified, but we believe that a study of the dietary patterns of Eastern countries with low ALS rates, such as China or

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Summary

Introduction

Academic Editors: Isabel Borrás and Jesús Lozano-Sánchez. First described in 1869 by neurologist Jean-Martin Charcot, Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that involves motor neurons (MNs) with onset between 50 and 65 years [1,2,3,4]. ALS may occur in a sporadic form, the most common (90–95% of cases), with no known hereditary component, or in a family-form (5–10% of cases) with a hereditary component, involving altered genes such as TAR DNA Binding. Protein (TARDBP or TDP43), Superoxide Dismutase 1 (SOD1), FUS RNA Binding Protein (FUS), and C9orf72-SMCR8 Complex Subunit (C9orf72) [5,6,7,8]. Mutations in SOD1 were prevalent in Scandinavia and mutations in TDP43 in Sardinia population [8]. Genetic susceptibility has been reported by association studies that revealed several potential

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