Amyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study
This 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), cerebrospi...
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| Veröffentlicht in: | European journal of epidemiology 2021, Vol.36 (1), p.81-88 |
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| creator | Yeung, Chris Ho Ching Lau, Kathleen Wen Din Au Yeung, Shiu Lun Schooling, C. Mary |
| description | This 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 tau
181
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 tau
181
were not associated with Alzheimer’s disease. For CSF Aβ
42
, 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
|
| doi_str_mv | 10.1007/s10654-020-00683-8 |
| format | Article |
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181
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 tau
181
were not associated with Alzheimer’s disease. For CSF Aβ
42
, 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 tau
181
(based on sample sizes ~ 3300) were not associated with Alzheimer’s disease using family history or clinically diagnosed cases while effects of CSF Aβ
42
were inconsistent between the family history and IGAP GWAS.</description><identifier>ISSN: 0393-2990</identifier><identifier>EISSN: 1573-7284</identifier><identifier>DOI: 10.1007/s10654-020-00683-8</identifier><identifier>PMID: 32929646</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aged ; Alzheimer Disease - blood ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer Disease - diagnosis ; Alzheimer Disease - genetics ; Alzheimer's disease ; Amplified Fragment Length Polymorphism Analysis ; Amyloid beta-Peptides - cerebrospinal fluid ; Amyloid beta-Peptides - genetics ; Amyloid beta-Peptides - metabolism ; Amyloid precursor protein ; Biomarkers - blood ; Cardiology ; Cerebrospinal fluid ; Epidemiology ; Family medical history ; Female ; Genetics ; Genome-wide association studies ; Genome-Wide Association Study ; Humans ; Infectious Diseases ; Male ; Medicine ; Medicine & Public Health ; Mendelian Randomization Analysis ; Middle Aged ; Neuro-Epidemiology ; Neurodegenerative diseases ; Oncology ; Outliers (statistics) ; Peptide Fragments ; Polymorphism, Single Nucleotide ; Proteins ; Public Health ; Randomization ; Sensitivity analysis ; Species ; Tau protein ; tau Proteins - blood ; tau Proteins - cerebrospinal fluid ; tau Proteins - metabolism ; Variance analysis ; β-Amyloid</subject><ispartof>European journal of epidemiology, 2021, Vol.36 (1), p.81-88</ispartof><rights>Springer Nature B.V. 2020</rights><rights>Springer Nature B.V. 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-e644fc81fed1b7f75a9c641a404a0958ce9a907ac79a871c19c530b8fd05e2853</citedby><cites>FETCH-LOGICAL-c375t-e644fc81fed1b7f75a9c641a404a0958ce9a907ac79a871c19c530b8fd05e2853</cites><orcidid>0000-0003-2753-1728</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10654-020-00683-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10654-020-00683-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32929646$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yeung, Chris Ho Ching</creatorcontrib><creatorcontrib>Lau, Kathleen Wen Din</creatorcontrib><creatorcontrib>Au Yeung, Shiu Lun</creatorcontrib><creatorcontrib>Schooling, C. Mary</creatorcontrib><title>Amyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study</title><title>European journal of epidemiology</title><addtitle>Eur J Epidemiol</addtitle><addtitle>Eur J Epidemiol</addtitle><description>This 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 tau
181
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 tau
181
were not associated with Alzheimer’s disease. For CSF Aβ
42
, 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 tau
181
(based on sample sizes ~ 3300) were not associated with Alzheimer’s disease using family history or clinically diagnosed cases while effects of CSF Aβ
42
were inconsistent between the family history and IGAP GWAS.</description><subject>Aged</subject><subject>Alzheimer Disease - blood</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer Disease - diagnosis</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer's disease</subject><subject>Amplified Fragment Length Polymorphism Analysis</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>Amyloid beta-Peptides - genetics</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyloid precursor protein</subject><subject>Biomarkers - blood</subject><subject>Cardiology</subject><subject>Cerebrospinal fluid</subject><subject>Epidemiology</subject><subject>Family medical history</subject><subject>Female</subject><subject>Genetics</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Infectious Diseases</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mendelian Randomization Analysis</subject><subject>Middle Aged</subject><subject>Neuro-Epidemiology</subject><subject>Neurodegenerative diseases</subject><subject>Oncology</subject><subject>Outliers (statistics)</subject><subject>Peptide Fragments</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Proteins</subject><subject>Public Health</subject><subject>Randomization</subject><subject>Sensitivity analysis</subject><subject>Species</subject><subject>Tau protein</subject><subject>tau Proteins - blood</subject><subject>tau Proteins - cerebrospinal fluid</subject><subject>tau Proteins - metabolism</subject><subject>Variance analysis</subject><subject>β-Amyloid</subject><issn>0393-2990</issn><issn>1573-7284</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kLtOHDEUhi0UBMvlBVJElmgomOR4bI_tdKtVAkgb0UBteT1nEm_mQuyZYqnyGnm9PAmGIYlEkeoU5_v_c_QR8pbBewagPiQGlRQFlFAAVJoXeo8smFS8UKUWb8gCuOFFaQwckqOUtgCgwcgDcshLU5pKVAtys-x27RDqCzq6ibq-pjGk73Ro6LJ9-Iahw_j7569E65DQJfxIHf2CfY1tcD2NmR-68ODGMPQ0jVO9OyH7jWsTnr7MY3L3-dPt6qpY31xer5brwnMlxwIrIRqvWYM126hGSWd8JZgTIFx-UXs0zoByXhmnFfPMeMlho5saJJZa8mNyPvfex-HHhGm0XUge29b1OEzJlkJkB4ZXT-jZK3Q7TLHP32VKCwABvMpUOVM-DilFbOx9DJ2LO8vAPum2s26bddtn3Vbn0LuX6mnTYf038sdvBvgMpLzqv2L8d_s_tY8kzYph</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Yeung, Chris Ho Ching</creator><creator>Lau, Kathleen Wen Din</creator><creator>Au Yeung, Shiu Lun</creator><creator>Schooling, C. 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Mary</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Amyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study</atitle><jtitle>European journal of epidemiology</jtitle><stitle>Eur J Epidemiol</stitle><addtitle>Eur J Epidemiol</addtitle><date>2021</date><risdate>2021</risdate><volume>36</volume><issue>1</issue><spage>81</spage><epage>88</epage><pages>81-88</pages><issn>0393-2990</issn><eissn>1573-7284</eissn><abstract>This 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 tau
181
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 tau
181
were not associated with Alzheimer’s disease. For CSF Aβ
42
, 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 tau
181
(based on sample sizes ~ 3300) were not associated with Alzheimer’s disease using family history or clinically diagnosed cases while effects of CSF Aβ
42
were inconsistent between the family history and IGAP GWAS.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>32929646</pmid><doi>10.1007/s10654-020-00683-8</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-2753-1728</orcidid></addata></record> |
| fulltext | fulltext |
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| ispartof | European journal of epidemiology, 2021, Vol.36 (1), p.81-88 |
| issn | 0393-2990 1573-7284 |
| language | eng |
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| subjects | Aged Alzheimer Disease - blood Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - diagnosis Alzheimer Disease - genetics Alzheimer's disease Amplified Fragment Length Polymorphism Analysis Amyloid beta-Peptides - cerebrospinal fluid Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Amyloid precursor protein Biomarkers - blood Cardiology Cerebrospinal fluid Epidemiology Family medical history Female Genetics Genome-wide association studies Genome-Wide Association Study Humans Infectious Diseases Male Medicine Medicine & Public Health Mendelian Randomization Analysis Middle Aged Neuro-Epidemiology Neurodegenerative diseases Oncology Outliers (statistics) Peptide Fragments Polymorphism, Single Nucleotide Proteins Public Health Randomization Sensitivity analysis Species Tau protein tau Proteins - blood tau Proteins - cerebrospinal fluid tau Proteins - metabolism Variance analysis β-Amyloid |
| title | Amyloid, tau and risk of Alzheimer’s disease: a Mendelian randomization study |
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