Alzheimer's disease is characterized by the pathognomonic presence of intracellular neurofibrillary tangles containing hyperphosphorylated tau protein and extracellular senile plaques primarily formed by β‐amyloid. Both the neurofibrillary tangles and the plaques formed by β‐amyloid 1‐42 are the final result of a chain of events that progressed along with the disease for a long time. Oxidative stress plays a fundamental role among those events as proven by the experiments carried out using animal models. This can be demonstrated since there are studies indicating that, although the formation of β‐amyloid is inhibited through different mechanisms (using drugs or specific antibodies), cognitive deficit is not prevented. In this chapter, we will focus on reviewing the role the chronic state of oxidative stress plays in the development of Alzheimer's disease and how the loss of redox balance induces a vicious cycle that may change normal signaling. As a consequence, there are alterations in multiple metabolic pathways that end up in the formation of hyperphosphorylated tau and insoluble β‐amyloid, leading to the advance of a progressive neurodegeneration process. This is characterized by neuronal dead, astrocytic changes, microglia activation, and the loss of brain repair.
Part of the book: Free Radicals and Diseases