No 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.

Silicon added to RP strongly counterbalanced the negative effect of high-cholesterol-ingestion, functioning as an active hypocholesterolemic, hypolipemic, and antioxidative dietary ingredient in aged rats.

Complement activation on cell surfaces leads to the massive deposition of C3b, iC3b, and C3dg, the main complement opsonins. Recognition of iC3b by complement receptor type 3 (CR3) fosters pathogen opsonophagocytosis by macrophages and the stimulation of adaptive immunity by complement-opsonized antigens. Here, we present the crystallographic structure of the complex between human iC3b and the von Willebrand A inserted domain of the α chain of CR3 (αI). The crystal contains two composite interfaces for CR3 αI, encompassing distinct sets of contiguous macroglobulin (MG) domains on the C3c moiety, MG1-MG2 and MG6-MG7 domains. These composite binding sites define two iC3b-CR3 αI complexes characterized by specific rearrangements of the two semi-independent modules, C3c moiety and TED domain. Furthermore, we show the structure of iC3b in a physiologically-relevant extended conformation. Based on previously available data and novel insights reported herein, we propose an integrative model that reconciles conflicting facts about iC3b structure and function and explains the molecular basis for iC3b selective recognition by CR3 on opsonized surfaces.