ABSTRACT
Just three years after Alois Alzheimer published the clinical and histopathological features of the rst case of presenile dementia in 1907 [1], Oskar Fischer hypothesized that inammation was present in the brains of patients with dementia [2]; however, only in the last two decades has this hypothesis been systematically studied and conrmed. Thanks to this relatively recent consideration, inammatory pathways are now essential to the discussion of the pathogenesis and progression of Alzheimer’s disease (AD). As in heart disease, diabetes, cancer, arthritis, and numerous other diseases, inammation plays a central role in the pathophysiology of AD, the most common neurodegenerative disorder of aging.
