β-amyloid (green) clumps in the blood vessels of control mice (above), but the vessels of rodents lacking TNFR1 are clear (below).
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...
The Rockefeller University Press
2007
The Rockefeller University Press
2007
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