Infection, Neuroinflammation and Interventions for Healthy Brain and Longevity

Alzheimer disease (AD) is a disastrous neurodegenerativeNeurodegenerative disease for which presently no consensus exists neither for the etiology nor for the efficacity of treatments. The amyloid hypothesis of the disease pathogenesis predominated during decades stating that amyloid beta (Aβ) formation and oligomerization is the major cause for AD. Recently, beside the amyloid plaques and neurofibrillary tangles, the neuroinflammationNeuroinflammation was added as a derivative of these misfolded proteins. However, the recent clinical failure of trials targeting the Aβ raised again the hypothesis of a possible infectious origin for AD. Even if this hypothesis was first evoked already by Alois Alzheimer, it is not yet fully accepted. Many studies have supported that microorganisms, including spirochetes, herpesviruses and Porphyromonas gingivalis play a role in AD and beta-amyloid peptide (Aβ) is an antimicrobial peptide. These data gave new impetus to the infectionInfection hypothesis. In this chapter we will discuss why the amyloid hypothesis by itself does not explain AD, how the infectionInfection hypothesis may induce AD, and what are the consequences for a healthy brain considering the numerous treatment avenues for improving the quality of lifeQuality of life of the older subjects.