Method. Scores on a Swedish version of the Wechsler Adult Intelligence Scale Information and Block Design scores from 461 OCTO-Twin Study participants with confirmed death dates were modeled using quadratic growth curve models Selleck E7080 including both age and distance from death at study entry, sex, education, and dementia diagnosis as covariates of initial performance and of linear and quadratic change over time.
Results. Information scores showed statistically significant
evidence of slight within-person acceleration of declines in the no dementia group. Individuals with incident dementia declined more quickly, and those who were closer to death at study baseline had a stronger acceleration. Block Design scores declined but did not show evidence of such acceleration either within or across individuals. Decline was faster in incident cases closer to death at study entry.
Discussion. Within-person evidence of terminal decline is not as strong as previously published between-person results. Strategies for focusing models on longitudinal aspects of available data and the extent to which lack
of within-person evidence for terminal decline may stem from common data limitations are discussed.”
“G protein-coupled receptor 17 (GPR17), the new P2Y-like receptor, is phylogenetically related to the P2Y and cysteinyl leukotriene MLN2238 mw receptors, and responds to both uracil nucleotides and cysteinyl leukotrienes. GPR17 has been proposed to be a damage sensor in ischemic stroke; however, its role in brain inflammation needs further detailed investigation. Here, we extended previous studies on the spatiotemporal profiles of GPR17 expression and localization, and their implications for brain injury after focal cerebral ischemia. We found that in the ischemic core, GPR17 mRNA and protein levels were upregulated at both 12-24 h and 7-14
days, but in the boundary zone the levels increased 7-14 days after reperfusion. The spatiotemporal pattern of GPR17 expression well matched the acute and late (subacute/chronic) responses in the ischemic brain. According to previous findings, in the acute phase, after ischemia (24 h), upregulated GPR17 was localized in injured neurons in the ischemic core and in a few microglia many in the ischemic core and boundary zone. In the late phase (14 days), it was localized in microglia, especially in activated (ED1-positive) microglia in the ischemic core, but weakly in most microglia in the boundary zone. No GPR17 was detectable in astrocytes. GPR17 knockdown by a small interfering RNA attenuated the neurological dysfunction, infarction, and neuron loss at 24 h, and brain atrophy, neuron loss, and microglial activation at 14 days after reperfusion. Thus, GPR17 might mediate acute neuronal injury and late microgliosis after focal cerebral ischemia. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.