Inflammation in Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disorder to date. Next to its classical histopathological characteristics such as deposition of fibrillogenic amyloid β peptides and neurofibrillary tangles, an inflammatory component of the disease has been identified. This article will review which cell types contribute to this phenomenon and which pro- and anti-inflammatory mediators are being released in the AD brain. Further, it will be discussed whether there are any known pathogenetic factors that may facilitate the induction and persistence of neuroinflammatory mechanisms. While neuroinflammation has mostly been quoted as a reaction to neurodegenerative events, more recent evidence suggests that it can feedback stimulate on neurodegenerative pathomechanisms including the generation of amyloid β peptides, thereby establishing a vicious and self-perpetuating cycle. Along this line, pro- and anti-inflammatory mechanisms may also contribute to the chronicity and duration of the disease. Therefore, anti-inflammatory treatment strategies should be evaluated as possible future therapeutics for AD.