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RISS 인기검색어
- 검색키워드
- 저자 : Thalamuthu, Anbupalam (검색결과 2 건)
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Lipnicki, Darren M.,Crawford, John D.,Dutta, Rajib,Thalamuthu, Anbupalam,Kochan, Nicole A.,Andrews, Gavin,Lima-Costa, M. Fernanda,Castro-Costa, Erico,Brayne, Carol,Matthews, Fiona E.,Stephan, Blossom Public Library of Science 2017 PLoS medicine Vol.14 No.3
<▼1><P><B>Background</B></P><P>The prevalence of dementia varies around the world, potentially contributed to by international differences in rates of age-related cognitive decline. Our primary goal was to investigate how rates of age-related decline in cognitive test performance varied among international cohort studies of cognitive aging. We also determined the extent to which sex, educational attainment, and apolipoprotein E ε4 allele (<I>APOE*4</I>) carrier status were associated with decline.</P><P><B>Methods and findings</B></P><P>We harmonized longitudinal data for 14 cohorts from 12 countries (Australia, Brazil, France, Greece, Hong Kong, Italy, Japan, Singapore, Spain, South Korea, United Kingdom, United States), for a total of 42,170 individuals aged 54–105 y (42% male), including 3.3% with dementia at baseline. The studies began between 1989 and 2011, with all but three ongoing, and each had 2–16 assessment waves (median = 3) and a follow-up duration of 2–15 y. We analyzed standardized Mini-Mental State Examination (MMSE) and memory, processing speed, language, and executive functioning test scores using linear mixed models, adjusted for sex and education, and meta-analytic techniques. Performance on all cognitive measures declined with age, with the most rapid rate of change pooled across cohorts a moderate -0.26 standard deviations per decade (SD/decade) (95% confidence interval [CI] [-0.35, -0.16], <I>p</I> < 0.001) for processing speed. Rates of decline accelerated slightly with age, with executive functioning showing the largest additional rate of decline with every further decade of age (-0.07 SD/decade, 95% CI [-0.10, -0.03], <I>p</I> = 0.002). There was a considerable degree of heterogeneity in the associations across cohorts, including a slightly faster decline (<I>p</I> = 0.021) on the MMSE for Asians (-0.20 SD/decade, 95% CI [-0.28, -0.12], <I>p</I> < 0.001) than for whites (-0.09 SD/decade, 95% CI [-0.16, -0.02], <I>p</I> = 0.009). Males declined on the MMSE at a slightly slower rate than females (difference = 0.023 SD/decade, 95% CI [0.011, 0.035], <I>p</I> < 0.001), and every additional year of education was associated with a rate of decline slightly slower for the MMSE (0.004 SD/decade less, 95% CI [0.002, 0.006], <I>p</I> = 0.001), but slightly faster for language (-0.007 SD/decade more, 95% CI [-0.011, -0.003], <I>p</I> = 0.001). <I>APOE*4</I> carriers declined slightly more rapidly than non-carriers on most cognitive measures, with processing speed showing the greatest difference (-0.08 SD/decade, 95% CI [-0.15, -0.01], <I>p</I> = 0.019). The same overall pattern of results was found when analyses were repeated with baseline dementia cases excluded. We used only one test to represent cognitive domains, and though a prototypical one, we nevertheless urge caution in generalizing the results to domains rather than viewing them as test-specific associations. This study lacked cohorts from Africa, India, and mainland China.</P><P><B>Conclusions</B></P><P>Cognitive performance declined with age, and more rapidly with increasing age, across samples from diverse ethnocultural groups and geographical regions. Associations varied across cohorts, suggesting that different rates of cognitive decline might contribute to the global variation in dementia prevalence. However, the many similarities and consistent associations with education and <I>APOE</I> genotype indicate a need to explore how international differences in associations with other risk factors such as genetics, cardiovascular health, and lifestyle are involved. Future studies should attempt to use multiple tests for each cognitive domain and feature populations from ethnocultural groups and geographical regions for which we lacked data.</P></▼1><▼2><P>In a collaborative cohort study, Darren Lipnicki and colleagues investigate associations between age-related cognitive decline and sex, education, and apoli
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Genome-wide average DNA methylation is determined <i>in utero</i>
Li, Shuai,Wong, Ee Ming,Dugué,, Pierre-Antoine,McRae, Allan F,Kim, Eunae,Joo, Ji-Hoon Eric,Nguyen, Tuong L,Stone, Jennifer,Dite, Gillian S,Armstrong, Nicola J,Mather, Karen A,Thalamuthu, Anbupal Oxford University Press 2018 International journal of epidemiology Vol.47 No.3
<P><B>Abstract</B></P><P><B>Background</B></P><P>Investigating the genetic and environmental causes of variation in genome-wide average DNA methylation (GWAM), a global methylation measure from the HumanMethylation450 array, might give a better understanding of genetic and environmental influences on methylation.</P><P><B>Methods</B></P><P>We measured GWAM for 2299 individuals aged 0 to 90 years from seven twin and/or family studies. We estimated familial correlations, modelled correlations with cohabitation history and fitted variance components models for GWAM.</P><P><B>Results</B></P><P>The correlation in GWAM for twin pairs was ∼0.8 at birth, decreased with age during adolescence and was constant at ∼0.4 throughout adulthood, with no evidence that twin pair correlations differed by zygosity. Non-twin first-degree relatives were correlated, from 0.17 [95% confidence interval (CI): 0.05–0.30] to 0.28 (95% CI: 0.08–0.48), except for middle-aged siblings (0.01, 95% CI: −0.10–0.12), and the correlation increased with time living together and decreased with time living apart. Spouse pairs were correlated in all studies, from 0.23 (95% CI: 0.3–0.43) to 0.31 (95% CI: 0.05–0.52), and the correlation increased with time living together. The variance explained by environmental factors shared by twins alone was 90% (95% CI: 74–95%) at birth, decreased in early life and plateaued at 28% (95% CI: 17–39%) in middle age and beyond. There was a cohabitation-related environmental component of variance.</P><P><B>Conclusions</B></P><P>GWAM is determined <I>in utero</I> by prenatal environmental factors, the effects of which persist throughout life. The variation of GWAM is also influenced by environmental factors shared by family members, as well as by individual-specific environmental factors.</P>
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