Browsing by Subject "cognitive decline"

Now showing 1 - 4 of 4
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    The Effects of Longitudinal White Matter Hyperintensity Change on Cognitive Decline and Cortical Thinning over Three Years
    (MDPI, 2020-08-17) Kim, Seung Joo; Lee, Dong Kyun; Jang, Young Kyoung; Jang, Hyemin; Kim, Si Eun; Cho, Soo Hyun; Kim, Jun Pyo; Jung, Young Hee; Kim, Eun-Joo; Na, Duk L.; Lee, Jong-Min; Seo, Sang Won; Kim, Hee Jin; Radiology and Imaging Sciences, School of Medicine
    White matter hyperintensity (WMH) has been recognised as a surrogate marker of small vessel disease and is associated with cognitive impairment. We investigated the dynamic change in WMH in patients with severe WMH at baseline, and the effects of longitudinal change of WMH volume on cognitive decline and cortical thinning. Eighty-seven patients with subcortical vascular mild cognitive impairment were prospectively recruited from a single referral centre. All of the patients were followed up with annual neuropsychological tests and 3T brain magnetic resonance imaging. The WMH volume was quantified using an automated method and the cortical thickness was measured using surface-based methods. Participants were classified into WMH progression and WMH regression groups based on the delta WMH volume between the baseline and the last follow-up. To investigate the effects of longitudinal change in WMH volume on cognitive decline and cortical thinning, a linear mixed effects model was used. Seventy patients showed WMH progression and 17 showed WMH regression over a three-year period. The WMH progression group showed more rapid cortical thinning in widespread regions compared with the WMH regression group. However, the rate of cognitive decline in language, visuospatial function, memory and executive function, and general cognitive function was not different between the two groups. The results of this study indicated that WMH volume changes are dynamic and WMH progression is associated with more rapid cortical thinning.
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    Higher blood cadmium level is associated with greater cognitive decline in rural Chinese adults aged 65 or older
    (Elsevier, 2021-02) Liu, Hang; Su, Liqin; Chen, Xi; Wang, Sisi; Cheng, Yibin; Lin, Shaobin; Ding, Liang; Liu, Jingyi; Chen, Chen; Unverzagt, Frederick W.; Hake, Ann M.; Jin, Yinlong; Gao, Sujuan; Psychiatry, School of Medicine
    Cadmium (Cd) exposure has been reported to have neurotoxic effects in animal studies and associated with increased Alzheimer's Disease mortality and lower cognitive function in cross-sectional and case-control studies. However, no results from longitudinal studies on Cd and cognitive decline are available. In this prospective cohort study, we recruited 1867 participants aged 65 years or older from rural areas in China, blood Cd and cognitive function were measured at baseline (2010−2012), and 1554 participants completed cognitive function tests during a 3-year follow-up (2013–2015). Cognitive function was evaluated using nine standardized cognitive tests: The Community Screening Instrument for Dementia, the CERAD Word List Learning, Word list recall, IU Story Recall, Animal Fluency Test, Boston Naming Test, Stick Design, Delayed Stick Design and the IU Token Test. Analysis of covariance models and logistic regression models were used to determine the association between Cd and standardized cognitive decline adjusting for covariates. The median blood Cd concentration of this study population was 2.12 μg/L, and the interquartile range was 1.42–4.64 μg/L. Significant association of higher Cd levels with lower cognitive scores were observed in five individual cognitive tests (Delayed Stick Design Test, Boston Naming Test, CERAD Word List Learning Test, Word List Recall Test and IU Story Recall Test) and the composite cognitive score adjusting for multi-covariates at baseline. Higher Cd levels were significantly associated with greater 3-year cognitive decline in Delayed Stick Design Test, Boston Naming Test, IU Token Test, Word List Recall Test and Composite cognitive score. For these cognitive tests, participants in the top two Cd quartile groups had significantly greater decline than those in the lowest Cd quartile group, while the two lowest Cd quartile groups were not significantly different. Our findings suggest that higher Cd exposure is associated with greater cognitive decline in older Chinese adults.
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    A multivariate finite mixture latent trajectory model with application to dementia studies
    (Taylor & Francis, 2016) Lai, Dongbing; Xu, Huiping; Katz, Barry; Koller, Daniel; Foroud, Tatiana; Gao, Sujuan; Department of Biostatistics, Richard M. Fairbanks School of Public Health
    Dementia patients exhibit considerable heterogeneity in individual trajectories of cognitive decline, with some patients showing rapid decline following diagnoses while others exhibiting slower decline or remaining stable for several years. Dementia studies often collect longitudinal measures of multiple neuropsychological tests aimed to measure patients’ decline across a number of cognitive domains. We propose a multivariate finite mixture latent trajectory model to identify distinct longitudinal patterns of cognitive decline simultaneously in multiple cognitive domains, each of which is measured by multiple neuropsychological tests. EM algorithm is used for parameter estimation and posterior probabilities are used to predict latent class membership. We present results of a simulation study demonstrating adequate performance of our proposed approach and apply our model to the Uniform Data Set from the National Alzheimer's Coordinating Center to identify cognitive decline patterns among dementia patients.
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    OVERCOMING THE AGE-ASSOCIATED DECLINE IN NEURAL STEM CELL PROLIFERATION
    (Office of the Vice Chancellor for Research, 2012-04-13) Romine, Jennifer; Gao, Xiang; Chen, Jinhui
    The U.S. population is aging. Age-related cognitive decline is a major public health problem. Developing an approach to treat or delay cognitive decline is critical. Neurogenesis by neural stem/progenitor cells (NSCs) in the hippocampus is related to cognitive function, and is greatly affected by the aging process. The molecular signaling that regulates age-related decline in neurogenesis is still poorly understood. Here we took the advantage of a transgenic mouse, Nestin-GFP, to assess neurogenesis and molecular signal-ing related to age-related decline in neurogenesis. We found that the total number of NSCs, including quiescent neural progenitors (QNPs) and amplify-ing neural progenitors (ANPs) decreased as the mice aged, but more im-portantly, ANPs are more significantly affected than QNPs, leading to further reduction in number and proliferation of ANPs. We further found that the mTOR signaling pathway is impaired in NSCs as mice age. Activating the mTOR signaling pathway through Ketamine injections increased NSC prolif-eration in aged mice. In contrast, inhibiting the activity of the mTOR signal-ing pathway by rapamycin is sufficient to reduce ANP proliferation in young mice. These results indicate that NSCs becomes more quiescent when the activity of mTOR signaling is compromised in aged mice, and stimulating the activity of mTOR signaling can overcome the age-associated decline in NSC proliferation. This data suggests that promoting stem cell proliferation to en-hance neurogenesis may be a potential approach for attenuating cognitive decline in the aging brain.This work was supported by funding from the Ralph W. and Grace M. Showalter Research Award, Indiana University Biological Research Grant, NIH grants RR025761 and 1R21NS072631-01A, and Undergraduate Research Opportunities Program (UROP).