Neuritic or senile plaques are extracellular protein deposits of fibrils and amorphous aggregates of ^-amyloid protein.12 This formed protein is central to the pathogenesis of AD. The ^-amyloid protein is present in a nontoxic, soluble form in human brains. In AD, conformational changes occur that render it insoluble and cause it to deposit into amorphous diffuse plaques associated with dystrophic neuritis.15 Over time, these deposits become compacted into plaques and the ^-amyloid protein becomes fibrillar and neurotoxic. Inflammation occurs secondary to clusters of astrocytes and microglia surrounding these plaques.

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