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Jan 10, 2013
 |  BC Innovations  |  Targets & Mechanisms

Targeting inflammation in AD

German researchers have implicated the inflammasome, an intracellular sensor of proinflammatory signaling, as a key player in Alzheimer's disease.1 The findings provide additional evidence that Alzheimer's disease could be treated with anti-inflammatory agents that act upstream of b-amyloid deposition.

The accumulation of b-amyloid (Ab) is thought to underlie the neurodegeneration at the heart of AD, and as a result most efforts to treat the disease have focused on directly blocking Ab production or the accumulation of Ab plaques.

Although the central role of Ab in AD is widely accepted, Michael Heneka, professor of clinical neuroscience at the University of Bonn, said academic researchers observed in the 1980s "that people in advanced age either have plaques or plaques plus inflammation."

However, it was unclear whether brain inflammation is a cause or consequence of AD. "Inflammation has really been the stepchild of the AD field. People would laugh and say that inflammation is a complete bystander that is secondary to disease," Heneka said.

Now, Heneka's team has found that AD progression in mice requires the Nlr...

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