Infection, Neuroinflammation and Interventions for Healthy Brain and Longevity
Résumé
Alzheimer disease (AD) is a disastrous neurodegenerative 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 neuroinflammation 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 infection hypothesis. In this
chapter we will discuss why the amyloid hypothesis by itself does not explain AD, how
the infection hypothesis may induce AD, and what are the consequences for a healthy
brain considering the numerous treatment avenues for improving the quality of life of the
older subjects.
Domaines
Neurobiologie
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