Nutrigenomics as strategy for neuronal health

Nutrigenomics through gene expression and epigenetic remodeling can program adult health. Diet during pregnancy and lactation (the first 1000 days of life) can modulate offspring’s epigenome leading to tissue specific variations during cell differentiation processes, and may define epigenetic marks associated with longterm effects on offspring neuronal health. Being epigenetics reversible, a healthy diet represents a fundamental opportunity, even after the first 1000 days of life, for maintaining cellular homeostasis. The positive impact of food (i.e. maternal milk, oily fish, fruit and vegetables, curcumin, tea) with its dietary flavonoids (i.e. sulforaphane, quercetin, lutein, resveratrol, carotenoids) and other bioactive compounds (i.e. docosahexanoic acid, melatonin etc.), will be reflected on chromatin structure modulation and DNA methylation which are associated with switching on/off of genes. An anti-inflammatory diet during early-life and across the whole life may represent a key strategy for influencing brain plasticity and for building an “epigenetic memory” useful in developing neuronal resilience against early-life stressors and to prevent age-related neurodegeneration

Overlapped metabolic and therapeutic links between Alzheimer and diabetes

Alzheimer's disease (AD) and diabetes are among the most common diseases associated with ageing. The pathology of AD is strongly associated with accumulated misfolding proteins that results in neuronal dysfunction within the brain. Diabetes, on the contrary, is characterised by altered insulin signaling that results in reduced glucose uptake, metabolic suppression of energy consuming cells and conversion of glucose to fat in the liver. Despite distinguishing features, these diseases share common elements and may in fact be viewed as fundamentally similar disorders that differ in magnitude of specific traits, primarily affected tissues and time of onset. In this review, we outline the fundamental basis of each of the two diseases and highlight similarities in their pathophysiology. Further ahead we will discuss these features in relation to the development of drugs to treat these two diseases, particularly AD, for which the development of therapeutic chemicals has proven to be particularly difficult. We conclude with comments on efforts to develop a simple organism, Caenorhabditis elegans, as a genetic model to be used to study the systems biology of diabetes and AD