350 research outputs found

    Correspondence of Roger Hedlund: Sat Tal Conference 1987

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    https://place.asburyseminary.edu/rogerhedlundpapers/1314/thumbnail.jp

    Correspondence of Roger Hedlund: CGRC Personnel 1982-1984

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    https://place.asburyseminary.edu/rogerhedlundpapers/1118/thumbnail.jp

    Roger Hedlund ARC2012 -002 - Finding Aid

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    https://place.asburyseminary.edu/findingaids/1018/thumbnail.jp

    Subject File of Roger Hedlund: Hindu Evangelization Conference 1990

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    https://place.asburyseminary.edu/rogerhedlundpapers/1293/thumbnail.jp

    Subject File of Roger Hedlund: CGRC-CGAI Constitutional Revision and Institutional Membership

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    https://place.asburyseminary.edu/rogerhedlundpapers/1278/thumbnail.jp

    Subject File of Roger Hedlund: Church Growth Activities in India 1976-1978

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    https://place.asburyseminary.edu/rogerhedlundpapers/1283/thumbnail.jp

    Correspondence of Roger Hedlund: CGRC Headquarters Project July-Sept 1985

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    https://place.asburyseminary.edu/rogerhedlundpapers/1126/thumbnail.jp

    Association study of cholesterol-related genes in Alzheimer's disease

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    Alzheimer's disease (AD) is a genetically complex disorder, and several genes related to cholesterol metabolism have been reported to contribute to AD risk. To identify further AD susceptibility genes, we have screened genes that map to chromosomal regions with high logarithm of the odds scores for AD in full genome scans and are related to cholesterol metabolism. In a European screening sample of 115 sporadic AD patients and 191 healthy control subjects, we analyzed single nucleotide polymorphisms in 28 cholesterol-related genes for association with AD. The genes HMGCS2, FDPS, RAFTLIN, ACAD8, NPC2, and ABCG1 were associated with AD at a significance level of P ≤ 0.05 in this sample. Replication trials in five independent European samples detected associations of variants within HMGCS2, FDPS, NPC2, or ABCG1 with AD in some samples (P = 0.05 to P = 0.005). We did not identify a marker that was significantly associated with AD in the pooled sample (n = 2864). Stratification of this sample revealed an APOE-dependent association of HMGCS2 with AD (P = 0.004). We conclude that genetic variants investigated in this study may be associated with a moderate modification of the risk for AD in some sample
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