ABSTRACT
Alzheimer’s disease (AD) is a progressive degenerative disease characterized by the gradual loss of cognitive function. Identified cellular defects include (a) increased oxidative stress, (b) chronic inflammation, (c) mitochondrial dysfunction, (d) Aß1-42 peptides generated from the cleavage of amyloid precursor protein (APP), (e) proteasome inhibition, (f) high cholesterol levels, (g) hyperphosphorylated tau protein, and (h) heritable mutations in APP, presenilin-1, and presenilin-2 genes. Analysis of studies suggests that increased oxidative damage precedes other biochemical and genetic defects. Oxidative damage, if not repaired, leads to chronic inflammation. Therefore, attenuation of oxidative stress and chronic inflammation may reduce the risk and improve management of AD. Alterations in the expressions of microRNAs are involved in the pathogenesis of AD. Reactive oxygen species (ROS) and pro-inflammatory cytokines, and antioxidants regulate the expression of microRNAs and their target proteins that cause neurodegeneration and neuroprotection, respectively. Effects of individual micronutrients in experimental models and human AD produced inconsistent results. In order to reduce oxidative stress and chronic inflammation, elevation of the antioxidant enzymes, and the dietary and endogenous antioxidants, is essential. A mixture of micronutrients that would achieve this goal for prevention, and in combination with standard therapy, for improved management of AD is proposed.
