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Article: Amyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study

TitleAmyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study
Authors
KeywordsAlzheimer’s disease
Amyloid
Tau
Mendelian randomization
Issue Date2021
PublisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0393-2990
Citation
European Journal of Epidemiology, 2021, v. 36 n. 1, p. 81-88 How to Cite?
AbstractThis study was carried out to assess the effect of amyloid and tau on Alzheimer’s disease using two-sample Mendelian randomization design. Genetic associations with plasma amyloid species (amyloid precursor protein, amyloid-like protein 2, serum amyloid P-component, amyloid beta peptide), cerebrospinal fluid (CSF) amyloid beta, total tau, and phosphorylated tau181 were extracted from the largest genome-wide association study (GWAS) available. Genetic associations with Alzheimer’s disease were obtained from a GWAS of proxy-cases based on family history of Alzheimer’s disease with 314,278 participants from the UK Biobank and a GWAS with clinically diagnosed Alzheimer’s disease from the International Genomics of Alzheimer’s Project (IGAP) with 21,982 cases and 41,944 controls. Estimates were obtained using inverse variance weighting with sensitivity analyses including MR-Egger, weighted median and MR-PRESSO. Presence of bias due to selective survival and competing risk was also considered. Plasma amyloid species, CSF total tau and phosphorylated tau181 were not associated with Alzheimer’s disease. For CSF Aβ42, no association was found using the proxy-cases but an inverse association was found after removing outliers with MR-PRESSO using IGAP. Higher genetically predicted (p < 1 × 10−5) plasma amyloid species, CSF total tau and phosphorylated tau181 (based on sample sizes ~ 3300) were not associated with Alzheimer’s disease using family history or clinically diagnosed cases while effects of CSF Aβ42 were inconsistent between the family history and IGAP GWAS.
Persistent Identifierhttp://hdl.handle.net/10722/290011
ISSN
2023 Impact Factor: 7.7
2023 SCImago Journal Rankings: 3.186
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYEUNG, CHC-
dc.contributor.authorLau, KWD-
dc.contributor.authorAu Yeung, SL-
dc.contributor.authorSchooling, CM-
dc.date.accessioned2020-10-22T08:20:40Z-
dc.date.available2020-10-22T08:20:40Z-
dc.date.issued2021-
dc.identifier.citationEuropean Journal of Epidemiology, 2021, v. 36 n. 1, p. 81-88-
dc.identifier.issn0393-2990-
dc.identifier.urihttp://hdl.handle.net/10722/290011-
dc.description.abstractThis study was carried out to assess the effect of amyloid and tau on Alzheimer’s disease using two-sample Mendelian randomization design. Genetic associations with plasma amyloid species (amyloid precursor protein, amyloid-like protein 2, serum amyloid P-component, amyloid beta peptide), cerebrospinal fluid (CSF) amyloid beta, total tau, and phosphorylated tau181 were extracted from the largest genome-wide association study (GWAS) available. Genetic associations with Alzheimer’s disease were obtained from a GWAS of proxy-cases based on family history of Alzheimer’s disease with 314,278 participants from the UK Biobank and a GWAS with clinically diagnosed Alzheimer’s disease from the International Genomics of Alzheimer’s Project (IGAP) with 21,982 cases and 41,944 controls. Estimates were obtained using inverse variance weighting with sensitivity analyses including MR-Egger, weighted median and MR-PRESSO. Presence of bias due to selective survival and competing risk was also considered. Plasma amyloid species, CSF total tau and phosphorylated tau181 were not associated with Alzheimer’s disease. For CSF Aβ42, no association was found using the proxy-cases but an inverse association was found after removing outliers with MR-PRESSO using IGAP. Higher genetically predicted (p < 1 × 10−5) plasma amyloid species, CSF total tau and phosphorylated tau181 (based on sample sizes ~ 3300) were not associated with Alzheimer’s disease using family history or clinically diagnosed cases while effects of CSF Aβ42 were inconsistent between the family history and IGAP GWAS.-
dc.languageeng-
dc.publisherSpringer Verlag Dordrecht. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0393-2990-
dc.relation.ispartofEuropean Journal of Epidemiology-
dc.rightsThis is a post-peer-review, pre-copyedit version of an article published in [insert journal title]. The final authenticated version is available online at: https://doi.org/[insert DOI]-
dc.subjectAlzheimer’s disease-
dc.subjectAmyloid-
dc.subjectTau-
dc.subjectMendelian randomization-
dc.titleAmyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study-
dc.typeArticle-
dc.identifier.emailAu Yeung, SL: ayslryan@hku.hk-
dc.identifier.emailSchooling, CM: cms1@hkucc.hku.hk-
dc.identifier.authorityAu Yeung, SL=rp02224-
dc.identifier.authoritySchooling, CM=rp00504-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10654-020-00683-8-
dc.identifier.pmid32929646-
dc.identifier.scopuseid_2-s2.0-85090937033-
dc.identifier.hkuros316610-
dc.identifier.volume36-
dc.identifier.issue1-
dc.identifier.spage81-
dc.identifier.epage88-
dc.identifier.isiWOS:000569309900001-
dc.publisher.placeNetherlands-
dc.identifier.issnl0393-2990-

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