TTR and Alzheimer disease: TTRis increasingly recognized to act as an Aβ scavengerin the brain, as indicated by the increased levels of this proteinin the CSF during aging,16 the expressionof TTR in the heat shock response in neurons,21 the concomitant reduction in the level of Aβ and TTR in theCSF in AD,16,18 and the colocalization of thetwo proteins in the senile plaques of the cortex and hippocampus inAD.11 In fact, it seems that TTR is upregulatedas a result of aging, stress, and as a means of protection againstthe aggregates of Aβ40/Aβ42 in thebrain and that it follows the fate of the CSF pool of Aβ.