5 research outputs found

    Cognitive and physical variable comparison between high Alzheimer’s disease (AD) polygenic risk, amyotrophic lateral sclerosis (ALS) polygenic risk, and frontotemporal dementia (FTD) polygenic risk, N for each group is shown.

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    <p>Cognitive and physical variable comparison between high Alzheimer’s disease (AD) polygenic risk, amyotrophic lateral sclerosis (ALS) polygenic risk, and frontotemporal dementia (FTD) polygenic risk, N for each group is shown.</p

    Heat map of associations between the polygenic profile scores for neurodegenerative disease and cognitive ability and physical health.

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    <p>Stronger associations are indicated by darker shades, red indicates a positive association, blue indicates a negative association. AD, Alzheimer’s disease; ALS, amyotrophic lateral sclerosis; FTD, frontotemporal dementia; TMT B-A, trail-making part B–part A; TMT B, trail making part B; TMT A, trail making part A; DSS, digit symbol substitution; VNR, verbal numerical reasoning; FVC, forced vital capacity; PEF, peak expiratory flow; FEV1, forced expiratory volume in 1s. *, significant association after FDR correction (p-value ≤ 0.018 (AD), 0.024 (ALS), or 0.0041 (FTD)). Full results can be found in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0198187#pone.0198187.s001" target="_blank">S1 Table</a>.</p

    Associations between polygenic risk scores for Alzheimer’s disease (FDR p-value ≤ 0.018), amyotrophic lateral sclerosis (FDR p-value ≤ 0.0024), and frontotemporal dementia (FDR p-value ≤ 0.0041), and cognitive and physical measures controlling for age, sex, assessment centre, genotyping batch and array and 10 genetic principal components for population structure.

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    <p>Associations between polygenic risk scores for Alzheimer’s disease (FDR p-value ≤ 0.018), amyotrophic lateral sclerosis (FDR p-value ≤ 0.0024), and frontotemporal dementia (FDR p-value ≤ 0.0041), and cognitive and physical measures controlling for age, sex, assessment centre, genotyping batch and array and 10 genetic principal components for population structure.</p

    COVID-19 Host Genetics Initiative. A first update on mapping the human genetic architecture of COVID-19

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    The COVID-19 pandemic continues to pose a major public health threat, especially in countries with low vaccination rates. To better understand the biological underpinnings of SARS-CoV-2 infection and COVID-19 severity, we formed the COVID-19 Host Genetics Initiative1. Here we present a genome-wide association study meta-analysis of up to 125,584 cases and over 2.5 million control individuals across 60 studies from 25 countries, adding 11 genome-wide significant loci compared with those previously identified2. Genes at new loci, including SFTPD, MUC5B and ACE2, reveal compelling insights regarding disease susceptibility and severity.</p
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