J. Neurosci. 30, 4528–4535 (2010)

Misfolded proteins implicated in Alzheimer's disease and prion disorders such as Creutzfeldt–Jacob disease may interact, making each disease worse.

Claudio Soto at the University of Texas Medical School at Houston and his colleagues introduced prions into normal mice and mice genetically predisposed to developing symptoms of Alzheimer's disease, such as amyloid plaques in the brain.

They found that prion disease developed more aggressively in Alzheimer's mice than in normal mice. Inoculated Alzheimer's mice also had many more plaques than did non-inoculated Alzheimer's animals. The results suggest that the presence of one protein-misfolding process increases the risk of a similar process being triggered for another protein.