<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rizzo, Toni</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Baek, Jean-Ha</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">UPR Activation Evaluated in Lewy Body Dementias and AD</style></title><secondary-title><style face="normal" font="default" size="100%">MD Conference Express</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014-07-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">13-14</style></pages><abstract><style  face="normal" font="default" size="100%">Even though they have distinct clinical, pathologic, and biochemical features, Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease, and less commonly prion disease are all characterized by misfolded protein aggregation in the brain and fatal neuronal loss. The unfolded protein response (UPR) is emerging as a common player in all neurodegenerative diseases. This article discusses a study that is investigating changes in the UPR pathway in deceased subjects with PD with dementia (PDD) and dementia with Lewy bodies in comparison with patients with AD and control subjects.</style></abstract><number><style face="normal" font="default" size="100%">15</style></number><volume><style face="normal" font="default" size="100%">14</style></volume></record></records></xml>