[Alzheimer's disease and methylenetetrahydrofolate reductase gene polymorphisms: a potential nutrigenomic approach for Mexico]. / La enfermedad de Alzheimer y los polimorfismos del gen metilenotetrahidrofolato reductasa: una potencial aproximación nutrigenómica en México.

The establishment of medical genomics in Mexico offers the possibility to study in a more comprehensive manner the etiological factors of different diseases, providing a global view of the interaction between the genome and the environment. Nutrition is recognized as a significant determinant in several diseases, yet its interaction with polymorphisms, and in general with the genome, has not been properly addressed Mexico has a high prevalence of polymorphisms of the methylenetetrahydrofolate reductase gene, and in both clinical and basic studies this has been associated with an increased susceptibility of developing Alzheimer's disease. We propose a potential nutrigenomic approach for the study of Alzheimer disease in Mexico.

Agephagy - Adapting Autophagy for Health During Aging.

Autophagy is a major cellular recycling process that delivers cellular material and entire organelles to lysosomes for degradation, in a selective or non-selective manner. This process is essential for the maintenance of cellular energy levels, components, and metabolites, as well as the elimination of cellular molecular damage, thereby playing an important role in numerous cellular activities. An important function of autophagy is to enable survival under starvation conditions and other stresses. The majority of factors implicated in aging are modifiable through the process of autophagy, including the accumulation of oxidative damage and loss of proteostasis, genomic instability and epigenetic alteration. These primary causes of damage could lead to mitochondrial dysfunction, deregulation of nutrient sensing pathways and cellular senescence, finally causing a variety of aging phenotypes. Remarkably, advances in the biology of aging have revealed that aging is a malleable process: a mild decrease in signaling through nutrient-sensing pathways can improve health and extend lifespan in all model organisms tested. Consequently, autophagy is implicated in both aging and age-related disease. Enhancement of the autophagy process is a common characteristic of all principal, evolutionary conserved anti-aging interventions, including dietary restriction, as well as inhibition of target of rapamycin (TOR) and insulin/IGF-1 signaling (IIS). As an emerging and critical process in aging, this review will highlight how autophagy can be modulated for health improvement.

Lithium suppresses Aß pathology by inhibiting translation in an adult Drosophila model of Alzheimer's disease.

The greatest risk factor for Alzheimer's disease (AD) is age, and changes in the ageing nervous system are likely contributors to AD pathology. Amyloid beta (Aß) accumulation, which occurs as a result of the amyloidogenic processing of amyloid precursor protein (APP), is thought to initiate the pathogenesis of AD, eventually leading to neuronal cell death. Previously, we developed an adult-onset Drosophila model of AD. Mutant Aß42 accumulation led to increased mortality and neuronal dysfunction in the adult flies. Furthermore, we showed that lithium reduced Aß42 protein, but not mRNA, and was able to rescue Aß42-induced toxicity. In the current study, we investigated the mechanism/s by which lithium modulates Aß42 protein levels and Aß42 induced toxicity in the fly model. We found that lithium caused a reduction in protein synthesis in Drosophila and hence the level of Aß42. At both the low and high doses tested, lithium rescued the locomotory defects induced by Aß42, but it rescued lifespan only at lower doses, suggesting that long-term, high-dose lithium treatment may have induced toxicity. Lithium also down-regulated translation in the fission yeast Schizosaccharomyces pombe associated with increased chronological lifespan. Our data highlight a role for lithium and reduced protein synthesis as potential therapeutic targets for AD pathogenesis.

[Depression and diabetes: from epidemiology to neurobiology]. / Depresión y diabetes: de la epidemiología a la neurobiología.

INTRODUCTION: Worldwide, diabetes mellitus and depression are among the most prevalent diseases in their respective fields, metabolism and psychiatry. However, there is evidence that patients with diabetes are at increased risk of developing depression, although a bidirectional relationship might also exist. AIM: To present a comprehensive review of the clinical, epidemiological, psychosocial, emotional, and neurobiological basis of the relation between diabetes and depression. DEVELOPMENT: Epidemiological studies indicate that there is not only an augmented risk of developing depression in diabetic patients, but that this association increases the morbidity and mortality of these patients. While there is a considerable number of clinical studies that support this relation, little is known about the neurochemical mechanisms that would constitute its biological basis. CONCLUSION: Alterations in monoamines (serotonin and noradrenaline), the increases in cortisol by the hypothalamus-pituitary-adrenal axis, and trophic agents such as the brain-derived neurotrophic factor, through glycogen synthase kinase-3, constitute some of the abnormalities documented in diabetic patients and in animal models that could explain the association between depression and diabetes. Additionally, we briefly consider the psychoemotional factors that might underlie the depression-diabetes relation. The effects (most of them deleterious) of the antidepressive therapy in glucometabolic control are also discussed.

[Nutritional genomics: an approach to the genome-environment interaction]. / Genómica nutricional: una aproximación de la interacción genoma-ambiente.

Nutritional genomics forms part of the genomic sciences and addresses the interaction between genes and the human diet, its influence on metabolism and subsequent susceptibility to develop common diseases. It encompasses both nutrigenomics, which explores the effects of nutrients on the genome, proteome and metabolome; and nutrigenetics, that explores the effects of genetic variations on the diet/disease interaction. A number of mechanisms drive the gene/diet interaction: elements in the diet can act as links for transcription factor receptors and after intermediary concentrations, thereby modifying chromatin and impacting genetic regulation; affect signal pathways, regulating phosphorylation of tyrosine in receptors; decrease signaling through the inositol pathway; and act through epigenetic mechanisms, silencing DNA fragments by methylation of cytosine. The signals generated by polyunsaturated fatty acids are so powerful that they can even bypass insulin mediated lipogenesis, stimulated by carbohydrates. Some fatty acids modify the expression of genes that participate in fatty acid transport by lipoproteins. Nutritional genomics has myriad possible therapeutic and preventive applications: in patients with enzymatic deficiencies; in those with a genetic predisposition to complex diseases such as dyslipidemia, diabetes and cancer; in those that already suffer these diseases; in those with altered mood or memory; during the aging process; in pregnant women; and as a preventive measure in the healthy population.

La enfermedad de Alzheimer y los polimorfismos del gen metilenotetrahidrofolato reductasa: una potencial aproximación nutrigenómica en México / Alzheimer's disease and methylenetetrahydrofolate reductase gene polymorphisms: a potential nutrigenomic approach for Mexico

El establecimiento de la medicina genómica en México oferta la posibilidad de una mirada más integral de los factores etiológicos de las enfermedades, incorporando en una visión global la interacción del genoma con el ambiente. La nutrición es reconocida como determinante para algunas enfermedades, pero su interacción con polimorfismos, y en general con el genoma, ha sido poco estudiada. En México se informa alta prevalencia de polimorfismos en el gen metilenotetrahidrofolato reductasa, y tanto estudios clínicos como básicos la han relacionado con aumento de susceptibilidad para el desarrollo de enfermedad de Alzheimer. Esto ofrece una potencial aproximación nutrigenómica en el país.

The establishment of medical genomics in Mexico offers the possibility to study in a more comprehensive manner the etiological factors of different diseases, providing a global view of the interaction between the genome and the environment. Nutrition is recognized as a significant determinant in several diseases, yet its interaction with polymorphisms, and in general with the genome, has not been properly addressed Mexico has a high prevalence of polymorphisms of the methylenetetrahydrofolate reductase gene, and in both clinical and basic studies this has been associated with an increased susceptibility of developing Alzheimer's disease. We propose a potential nutrigenomic approach for the study of Alzheimer disease in Mexico.

Genómica nutricional: una aproximación de la interacción genoma-ambiente: [revisión] / Nutritional genomics: an approach to the genome-environment interaction: [review]

Nutritional genomics forms part of the genomic sciences and addresses the interaction between genes and the human diet, its influence on metabolism and subsequent susceptibility to develop common diseases. It encompasses both nutrigenomics, which explores the effects of nutrients on the genome, proteome and metabolome; and nutrigenetics, that explores the effects of genetic variations on the diet/disease interaction. A number of mechanisms drive the gene/diet interaction: elements in the diet can act as links for transcription factor receptors and alter intermediary concentrations, thereby modifying chromatin and impacting genetic regulation; affect signal pathways, regulating phosphorylation of tyrosine in receptors; decrease signaling through the inositol pathway; and act through epigenetic mechanisms, silencing DNA fragments by methylation of cytosine. The signals generated by polyunsaturated fatty acids are so powerful that they can even bypass insulin mediated lipogenesis, stimulated by carbohydrates. Some fatty acids modify the expression of genes that participate in fatty acid transport  by lipoproteins. Nutritional genomics has myriad possible therapeutic and preventive applications: in patients with enzymatic deficiencies; in those with a genetic predisposition to complex diseases such as dyslipidemia, diabetes and cancer; in those that already suffer these diseases; in those with altered mood or memory; during the aging process; in pregnant women; and as a preventive measure in the healthy population.