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        Enhancement of the Hall Mobility in Hydrogen-ion-irradiated ZnO Films

        Changsoo Yeo,정권범,박진성,Jong Han Song 한국물리학회 2012 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.60 No.3

        RF-sputtered ZnO films were irradiated with hydrogen ions by using an ion accelerator at 110 keV. The physical and the electrical characteristics of the irradiated ZnO films were studied as functions of the hydrogen-ion irradiation dose. The Hall measurement indicated that the carrier concentration had small changes regardless of irradiated hydrogen amount, but the mobility was dramatically enhanced after irradiation of 10<sup>15</sup> atoms/cm<sup>2</sup>. Even when the irradiated hydrogen dose was increased, the crystalline structure had no transformation and the composition was preserved. On the other hand, the electronic structure, measured by using X-ray absorption spectroscopy, exhibited a modification of the molecular orbital structure in the ZnO films irradiated at doses above 10<sup>15</sup> atoms/cm<sup>2</sup>. These distortions of the molecular orbital in the conduction band could lead to a mobility enhancement without a structural transformation.

      • Higher education affects accelerated cortical thinning in Alzheimer's disease: a 5-year preliminary longitudinal study

        Cho, Hanna,Jeon, Seun,Kim, Changsoo,Ye, Byoung Seok,Kim, Geon Ha,Noh, Young,Kim, Hee Jin,Yoon, Cindy W,Kim, Yeo Jin,Kim, Jung-Hyun,Park, Sang Eon,Kim, Sung Tae,Lee, Jong-Min,Kang, Sue J.,Suh, Mee Kyun Cambridge University Press 2015 INTERNATIONAL PSYCHOGERIATRICS - Vol.27 No.1

        <B>ABSTRACT</B><B>Background:</B><P>Epidemiological studies have reported that higher education (HE) is associated with a reduced risk of incident Alzheimer's disease (AD). However, after the clinical onset of AD, patients with HE levels show more rapid cognitive decline than patients with lower education (LE) levels. Although education level and cognition have been linked, there have been few longitudinal studies investigating the relationship between education level and cortical decline in patients with AD. The aim of this study was to compare the topography of cortical atrophy longitudinally between AD patients with HE (HE-AD) and AD patients with LE (LE-AD).</P><B>Methods:</B><P>We prospectively recruited 36 patients with early-stage AD and 14 normal controls. The patients were classified into two groups according to educational level, 23 HE-AD (>9 years) and 13 LE-AD (≤9 years).</P><B>Results:</B><P>As AD progressed over the 5-year longitudinal follow-ups, the HE-AD showed a significant group-by-time interaction in the right dorsolateral frontal and precuneus, and the left parahippocampal regions compared to the LE-AD.</P><B>Conclusion:</B><P>Our study reveals that the preliminary longitudinal effect of HE accelerates cortical atrophy in AD patients over time, which underlines the importance of education level for predicting prognosis.</P>

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      • Relative impact of amyloid-β, lacunes, and downstream imaging markers on cognitive trajectories

        Kim, Hee Jin,Yang, Jin Ju,Kwon, Hunki,Kim, Changsoo,Lee, Jong Min,Chun, Phillip,Kim, Yeo Jin,Jung, Na-Yeon,Chin, Juhee,Kim, Seonwoo,Woo, Sook-young,Choe, Yearn Seong,Lee, Kyung-Han,Kim, Sung Tae,Kim, Oxford University Press 2016 Brain Vol.139 No.9

        <P>Amyloid-beta deposition and cerebral small vessel disease are major contributors to age-related cognitive decline. In a longitudinal study of mild cognitive impairment, Kim et al. show that amyloid-beta and lacunes have differing effects on cognitive trajectories. Amyloid-beta has a greater impact on memory, and lacune number on frontal-executive function.Amyloid-beta and cerebral small vessel disease are the two major causes of cognitive impairment in the elderly. However, the underlying mechanisms responsible for precisely how amyloid-beta and cerebral small vessel disease affect cognitive impairment remain unclear. We investigated the effects of amyloid-beta and lacunes on downstream imaging markers including structural network and cortical thickness, further analysing their relative impact on cognitive trajectories. We prospectively recruited a pool of 117 mild cognitive impairment patients (45 amnestic type and 72 subcortical vascular type), from which 83 patients received annual follow-up with neuropsychological tests and brain magnetic resonance imaging for 3 years, and 87 patients received a second Pittsburgh compound B positron emission tomography analysis. Structural networks based on diffusion tensor imaging and cortical thickness were analysed. We used linear mixed effect regression models to evaluate the effects of imaging markers on cognitive decline. Time-varying Pittsburgh compound B uptake was associated with temporoparietal thinning, which correlated with memory decline (verbal memory test, unstandardized beta = -0.79, P < 0.001; visual memory test, unstandardized beta = -2.84, P = 0.009). Time-varying lacune number was associated with the degree of frontoparietal network disruption or thinning, which further affected frontal-executive function decline (Digit span backward test, unstandardized beta = -0.05, P = 0.002; Stroop colour test, unstandardized beta = -0.94, P = 0.008). Of the multiple imaging markers analysed, Pittsburgh compound B uptake and the number of lacunes had the greatest association with memory decline and frontal-executive function decline, respectively: Time-varying Pittsburgh compound B uptake (standardized beta = -0.25, P = 0.010) showed the strongest effect on visual memory test, followed by time-varying temporoparietal thickness (standardized beta = 0.21, P = 0.010) and time-varying nodal efficiency (standardized beta = 0.17, P = 0.024). Time-varying lacune number (standardized beta = -0.25, P = 0.014) showed the strongest effect on time-varying digit span backward test followed by time-varying nodal efficiency (standardized beta = 0.17, P = 0.021). Finally, time-varying lacune number (beta = -0.22, P = 0.034) showed the strongest effect on time-varying Stroop colour test followed by time-varying frontal thickness (standardized beta = 0.19, P = 0.026). Our multimodal imaging analyses suggest that cognitive trajectories related to amyloid-beta and lacunes have distinct paths, and that amyloid-beta or lacunes have greatest impact on cognitive decline. Our results provide rationale for the targeting of amyloid-beta and lacunes in therapeutic strategies aimed at ameliorating cognitive decline.</P>

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