ABSTRACT
Alzheimer’s disease (AD) is a multifactorial, neurodegenerative disorder, characterized by progressive memory loss and cognitive impairment. Neuropathological heterogeneity is observed as senile plaques, composed of aggregated amyloid beta peptides and neurofibrillary tangles, consisting of aggregated tau proteins, result in the selective degeneration of the hippocampus and selected areas of the neocortex. Genetic etiological factors, including mutations and polymorphisms increasing the risk of developing AD, are associated with overexpression or impaired clearance of pathological proteins or with increased oxidative stress and inflammation in the brain. Such genetic mutations account for only 5% of total AD cases. The remaining 95% are sporadic in nature and are age dependent, implying that environmental factors, rather than genetic ones, could play a prominent role in the pathogenesis of AD. This chapter discusses the involvement of various epigenetic mechanisms implicated in the pathogenesis of AD, and how dietary regimes could be adopted for the treatment or prevention of neurodegeneration in AD in the future.
