β-amyloid (green) clumps in the blood vessels of control mice (above), but the vessels of rodents lacking TNFR1 are clear (below).

Areceptor that incites cell suicide also promotes the accumulation of β-amyloid plaques in Alzheimer's disease (AD), as He et al. show on page 829. In mice prone to the brain buildups, eliminating the receptor cut the number of plaques and spared memory. The results point to new treatments for the incurable disease.

As plaques of β-amyloid collect in the brains of AD patients, large numbers of neurons die. Scientists suspect that this devastation stems from abnormal processing of APP, which leads to too much β-amyloid, or out-of-control inflammation—or a combination of the two.

A potential link between these two mechanisms is the tumor necrosis factor type 1 death receptor (TNFR1), which triggers brain cells to kill themselves. TNF-α, which is activated during brain...

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