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Alzheimer disease (AD) is characterized by the progressive accumulation of amyloid β protein (Aβ) in areas of the brain serving cognitive functions such as memory and language. The first of two separate reports (see the related articles beginning on pages 415 and 440) reveals that intrinsic T cell reactivity to the self-antigen Aβ exists in many humans and increases with age. This finding has implications for the design of Aβ vaccines. The second report demonstrates that a number of FDA-approved nonsteroidal anti-inflammatory drugs are capable of lowering Aβ levels in mice. The work suggests that further testing of the therapeutic utility of these types of compounds for the potential treatment of AD is warranted.