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Search: onr:"swepub:oai:DiVA.org:uu-97804" > Does APOE explain t...

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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003760naa a2200589 4500
001oai:DiVA.org:uu-97804
003SwePub
008081121s2008 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:117572934
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-978042 URI
0247 a https://doi.org/10.1002/ajmg.b.306812 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1175729342 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Blom, Elin Susanneu Uppsala universitet,Geriatrik4 aut
2451 0a Does APOE explain the linkage of Alzheimer’s disease to chromosome 19q13?
264 c 2007-12-27
264 1b Wiley,c 2008
338 a print2 rdacarrier
520 a We have studied the impact of the apolipoprotein E gene (APOE) on the chromosome 19 linkage peak from an analysis of sib-pairs affected by Alzheimer's disease. We genotyped 417 affected sib-pairs (ASPs) collected in Sweden and Norway (SWE), the UK and the USA for 10 microsatellite markers on chromosome 19. The highest Zlr (3.28, chromosome-wide P-value 0.036) from the multi-point linkage analysis was located approximately 1 Mb from APOE, at marker D19S178. The linkage to chromosome 19 was well explained by APOE in the whole sample as well as in the UK and USA subsamples, as identity by descent (IBD) increased with the number of epsilon 4 alleles in ASPs. There was a suggestion from the SWE subsample that linkage was higher than would be expected from APOE alone, although the test for this did not reach formal statistical significance. There was also a significant age at onset (aao) effect on linkage to chromosome 19q13 in the whole sample, which manifested itself as increased IBD sharing in relative pairs with lower mean aao. This effect was partially, although not completely, explained by APOE. The aao effect varied considerably between the different subsamples, with most of the effect coming from the UK sample. The other samples showed smaller effects in the same direction, but these were not significant.
653 a Alzheimer's disease
653 a APOE
653 a linkage
653 a age at onset
653 a apolipoprotein E
653 a MEDICINE
653 a MEDICIN
7001 a Holmans, Peter4 aut
7001 a Arepalli, Sampath4 aut
7001 a Adighibe, Omanma4 aut
7001 a Hamshere, Marian L.4 aut
7001 a Gatz, Margaret4 aut
7001 a Pedersen, Nancy L.u Karolinska Institutet4 aut
7001 a Bergem, A. L. Mina4 aut
7001 a Owen, Michael J.4 aut
7001 a Hollingworth, Paul4 aut
7001 a Goate, Alison4 aut
7001 a Williams, Julie4 aut
7001 a Lannfelt, Larsu Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)lalan021
7001 a Hardy, John4 aut
7001 a Wavrant-De Vrièze, Fabienne4 aut
7001 a Glaser, Annau Uppsala universitet,Geriatrik4 aut0 (Swepub:uu)angla622
7102 a Uppsala universitetb Geriatrik4 org
7730 t American Journal of Medical Genetics Part B: Neuropsychiatric Genetics American Journal of Medical Genetics Part B: Neuropsychiatric Geneticsd : Wileyg 147B:6, s. 778-83q 147B:6<778-83x 1552-485X
7730 t American Journal of Medical Genetics Part B: Neuropsychiatric Geneticsd : Wileyg 147B:6, s. 778-83q 147B:6<778-83x 1552-4841
8564 u https://europepmc.org/articles/pmc2726752?pdf=render
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-97804
8564 8u https://doi.org/10.1002/ajmg.b.30681
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:117572934

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