Inflammatory Pathways

Alzheimer’s disease (AD) is a dementing illness characterized clinically by global intellectual decline and pathologically by a profusion of microscopic brain lesions containing extracellular amyloid in a β-pleated sheet conformation (β-amyloid) associated with abnormal (dystrophic) neuntes. These neuritic β-amyloid plaques are thought to originate as otherwise undistinguished deposits of amyloid protein—diffuse nonneuritic plaques. With condensation of this amyloid, accompanied by the appearance of dystrophic neurites, these amyloid deposits evolve into neuritic plaques containing both diffuse amyloid and β-amyloid (diffuse neuritic plaques). With further evolution, amyloid condenses into a central compact core of β-amyloid within the larger deposit of diffuse amyloid, yielding a dense core neuritic plaque. Continued condensation apparently is accompanied by a loss of associated diffuse amyloid as well as neuritic elements, yielding a dense core of β-amyloid. These dense core, nonneuritic plaques (sometimes referred to as burned-out plaques) are thought to represent an end stage of plaque evolution (1) (for schematic representation of plaque progression, please see Fig. 1A). These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.