Abstract
The prevalence of degenerative diseases has risen in western countries. Growing evidence suggests that demenia and other cognition affectations are associated with ambient factors including specific nutrients, food ingredients or specific dietary patterns. Mediterranean diet adherence has been associated with various health benefits and decreased risk of many diseases, including neurodegenerative disorders. Beer, as part of this protective diet, contains compounds such as silicon and hops that could play a major role in preventing brain disorders. In this review, different topics regarding Mediterranean diet, beer and the consumption of their main compounds and their relation to neurological health have been addressed. Taking into account published results from our group and other studies, the hypothesis linking aluminum intoxication with dementia and/or Alzheimer’s disease and the potential role of regular beer has also been considered. Beer, in spite of its alcohol content, may have some health benefits; nonetheless, its consumption is not adequate for all subjects. Thus, this review analyzed some promising results of non-alcoholic beer on several mechanisms engaged in neurodegeneration such as inflammation, oxidation, and cholinesterase activity, and their contribution to the behavioral modifications induced by aluminum intoxication. The review ends by giving conclusions and suggesting future topics of research related to moderate beer consumption and/or the consumption of its major compounds as a potential instrument for protecting against neurodegenerative disease progression and the need to develop nutrigenetic and nutrigenomic studies in aged people and animal models.
Highlights
Increased lifespan in western countries has resulted in an impressively increased frequency of neurodegenerative diseases, the most common one being Alzheimer’s disease [1]
Noremberg et al [18] showed that intraperitoneal administration of silicon in similar concentrations to those found in parenteral nutrition reduces the harmful effects of increased lipoperoxides (LPO) in rat brain induced by long-term aluminum exposure
Aluminum induces several mechanisms engaged through mechanisms mechanisms that that mainly tau phosphorylation, amyloid beta peptide (Aβ) accumulation, accumulation, through mainly involve involve apoptosis, apoptosis, tau phosphorylation, Aβ
Summary
Increased lifespan in western countries has resulted in an impressively increased frequency of neurodegenerative diseases, the most common one being Alzheimer’s disease [1]. The link between obesity and/or the metabolic syndrome with neurodegenerative diseases was proposed [8,9] Along this line, Nuzzo et al [10,11] evaluated how obesity and Alzheimer’s disease markers are associated with inflammation, adipokine dyshomeostasis, oxidative stress, mitochondrial dysfunction, and neurodegeneration improvement in the frame of an insulin resistance model or in a functional ingredient-enriched high fat diet intervention,. Nuzzo et al [10,11] evaluated how obesity and Alzheimer’s disease markers are associated with inflammation, adipokine dyshomeostasis, oxidative stress, mitochondrial dysfunction, and neurodegeneration improvement in the frame of an insulin resistance model or in a functional ingredient-enriched high fat diet intervention, Other factors such as chronodisruption [12], autophagy capacity [13], or mitochondriogenesis [14] have been proposed to influence cognitive disorders. While APO-E remains the strongest predictor of Alzheimer’s disease, aging, diabetes mellitus, smoking habits, and lower socioeconomical engagement, among others, are associated with increased risk of Alzheimer’s development [20,21]
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