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Alzheimer΄s disease (AD) is the most frequent neurodegenerative disease and the most common cause of dementia in humans. Clinically, the classic and most frequent initial symptom is impaired short-term memory that progresses to profound memory failure. AD neuropathology exhibits two hallmark features: (1) senile plaques containing depositions of beta-amyloid protein and (2) neurofibrillary tangles (NFT). Quantitative neuropathological evaluation in early AD shows significant neuronal loss in brain memory regions. Genetic studies demonstrate that aberrant proteolytic processing of the amyloid precursor protein (APP) leads to 1–40 and 1–42 amyloid-β peptide (Aβ) fragments capable of causing AD pathology. However, the mechanisms by which amyloid proteins lead to plaque deposition, NFT, and neuronal cell death is incompletely understood. Thus, the objective of this chapter is to review what is known about disease mechanisms with a focus on the role played by neuroimmune interactions in neurodegenerative processes. [ABSTRACT FROM AUTHOR]