Neuroinflammatory Environments Promote Amyloid-ß Deposition and Posttranslational Modification

Indisputable evidence indicates that an inflammatory response is associated with neuron and neurite damage and the deposition of amyloid s (As) and neurofibrillary tangles (NFT) in Alzheimer disease (AD) (see, ref. 1 for a comprehensive review). Just as in the periphery, where degenerating tissue and insoluble materials (resulting from trauma, embolism, and rupture) promote inflammation, these classical stimulants also promote inflammation in the AD brain. From a spatio-temporal perspective, the stimuli promoting neuroinflammation are microlocalized and are present from early preclinical to the terminal stages of AD. Likewise, the upregulation of acute-phase proteins, complement, cytokines, and other inflammatory mediators also is microlocalized and chronic.