Potential preventive disease-modifying pharmacological strategies to delay late onset Alzheimer's disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated Tau protein. Over the years, AD has been classified in two subgroups: early onset or familial AD and late onset or sporadic AD. On the one hand, familial AD has been described to be the result of genetic mutations that cause, in some cases, for the overproduction of amyloid β. On the other, the cause of late onset or sporadic AD is still unclear even though several hypotheses have been proposed to explain the process of severe and progressive memory and cognitive loss. In the present review, some of the current hypotheses that try to explain the origin of late onset or sporadic AD have been summarized. Also, their potential implication in the development of new drugs for the presymptomatic treatment of late onset or sporadic AD has been considered.