Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative inflammatory disease which in Western society mainly accounts for clinical dementia. AD has been linked to inflammation and oxidative stress. Neuro-pathological hallmarks are senile plaques, resulting from the accumulation of several proteins and an inflammatory reaction around deposits of amyloid, a fibrillar protein, Abeta, product of cleavage of a much larger protein, the beta-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, due to the accumulation of Abeta peptide, is the main pathogenetic mechanism. Inflammation clearly occurs in pathologically vulnerable regions of AD and several inflammatory factors influencing AD development, i.e. environmental factors (pro-inflammatory phenotype) and/or genetic factors (pro-inflammatory genotype) have been described. In particular, genetic factors seem to be involved in AD pathophysiology, as demonstrated by molecular genetic and epidemiological studies identifying numerous gene polymorphisms as susceptibility AD modifiers. Several reports have suggested that the risk of AD is substantially influenced by polymorphisms in the promoter region, and other untranslated regions, of genes encoding inflammatory mediators. The better understanding of different molecular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Given these considerations, in our laboratory, we are evaluating whether pro-inflammatory alleles are risk factors for AD. To this purpose, we are performing genetic studies of some polymorphic inflammatory molecules by PCR and meta-analyses of cytokine polymorphisms. The results demonstrate that pro-inflammatory SNPs of inflammatory genes COX, 5-LO, TLR4, IL-1beta, TNF-alpha are significantly increased in patients when compared to healthy controls. On the other hand, irrespective of the source and mechanisms that lead to the generation of reactive oxygen species, mammalian cells have developed highly regulated inducible defensive systems, whose cytoprotective functions are essential in terms of cell survival. When appropriately activated, each one of these systems has the possibility to restore cellular homeostasis and rebalance redox equilibrium. Activation of antioxidant pathways is particularly important for tissue with relatively weak endogenous antioxidant defences, such as the brain. Increasing evidences, in fact, support the notion that reduction of cellular expression and activity of antioxidant proteins and consequent augment of oxidative stress are fundamental causes for ageing processes and neurodegenerative diseases., including AD. The genetic studies are going to permit the detection of a risk profile which will potentially allow both the early identification of individuals susceptible to disease and the possible design or utilize of drugs at the right dose for a desired effect, i.e., a pharmacogenomic approach for AD. On the other hand, available data on the involvement of curcumin in restoring cellular homeostasis and rebalancing redox equilibrium, suggest that curcumin might be an useful adjunct in the treatment of neurodegenerative diseases, such as AD.