[Alzheimer's disease, neuro-inflammation, and herpes viruses, a path that traces its way]

Infection of the brain with various types of pathogens, and the resulting inflammatory response, is becoming increasingly important in our understanding of the etiology of Alzheimer's disease (AD). The fact that several genes identified as risk factors are actually involved in the modulation of the immune response, as well as the very diversity of the infectious agents identified as possible actors in the evolution of this disease, argue in favor of the neuro-inflammatory hypothesis, as does the demonstration that the protein Aβ, one of the most important markers of AD, is an antimicrobial peptide. Among others, herpes viruses (mainly, but not only, HSV-1), which can establish latent infections in brain neurons, especially in the elder population, punctuated by episodes of reactivation following stress or immunosuppression, appear as very strong candidates to play an etiological role, if only as cofactors, of AD. Recent results show that, in human and rat neurons, infection with HSV-1 increases the formation of Aβ along the amyloidogenic pathway, as well as the phosphorylation of Tau proteins, another essential marker of AD. The growing evidence that chronic infections and defense mechanisms, including inflammatory processes, are at the heart of AD, warrants reviewing antiviral drugs such as acyclovir, and possibly vaccination, as potential avenues for AD control.