Physical activity and risk of Alzheimer disease: A 2-sample mendelian randomization study
OBJECTIVEEvidence from observational studies for the effect of physical activity on the risk of Alzheimer disease (AD) is inconclusive. We performed a 2-sample mendelian randomization analysis to examine whether physical activity is protective for AD. METHODSSummary data of genome-wide association s...
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| Veröffentlicht in: | Neurology 2020-09, Vol.95 (13), p.e1897-e1905 |
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| container_issue | 13 |
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| container_title | Neurology |
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| creator | Baumeister, Sebastian E. Karch, André Bahls, Martin Teumer, Alexander Leitzmann, Michael F. Baurecht, Hansjörg |
| description | OBJECTIVEEvidence from observational studies for the effect of physical activity on the risk of Alzheimer disease (AD) is inconclusive. We performed a 2-sample mendelian randomization analysis to examine whether physical activity is protective for AD.
METHODSSummary data of genome-wide association studies on physical activity and AD were used. The primary study population included 21,982 patients with AD and 41,944 cognitively normal controls. Eight single nucleotide polymorphisms (SNPs) known at p < 5 × 10 to be associated with average accelerations and 8 SNPs associated at p < 5 × 10 with vigorous physical activity (fraction of accelerations >425 milligravities) served as instrumental variables.
RESULTSThere was no association between genetically predicted average accelerations with the risk of AD (inverse variance weighted odds ratio [OR] per SD increment1.03, 95% confidence interval 0.97–1.10, p = 0.332). Genetic liability for fraction of accelerations >425 milligravities was unrelated to AD risk.
CONCLUSIONThe present study does not support a causal association between physical activity and risk of AD. |
| doi_str_mv | 10.1212/WNL.0000000000010013 |
| format | Article |
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METHODSSummary data of genome-wide association studies on physical activity and AD were used. The primary study population included 21,982 patients with AD and 41,944 cognitively normal controls. Eight single nucleotide polymorphisms (SNPs) known at p < 5 × 10 to be associated with average accelerations and 8 SNPs associated at p < 5 × 10 with vigorous physical activity (fraction of accelerations >425 milligravities) served as instrumental variables.
RESULTSThere was no association between genetically predicted average accelerations with the risk of AD (inverse variance weighted odds ratio [OR] per SD increment1.03, 95% confidence interval 0.97–1.10, p = 0.332). Genetic liability for fraction of accelerations >425 milligravities was unrelated to AD risk.
CONCLUSIONThe present study does not support a causal association between physical activity and risk of AD.</description><identifier>ISSN: 0028-3878</identifier><identifier>EISSN: 1526-632X</identifier><identifier>DOI: 10.1212/WNL.0000000000010013</identifier><identifier>PMID: 32680943</identifier><language>eng</language><publisher>United States: American Academy of Neurology</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer Disease - genetics ; Biological Specimen Banks ; Case-Control Studies ; Exercise ; Female ; Genetic Predisposition to Disease - genetics ; Genome-Wide Association Study - statistics & numerical data ; Humans ; Male ; Mendelian Randomization Analysis ; Middle Aged ; Null Hypothesis ; Polymorphism, Single Nucleotide ; Risk Factors</subject><ispartof>Neurology, 2020-09, Vol.95 (13), p.e1897-e1905</ispartof><rights>American Academy of Neurology</rights><rights>2020 American Academy of Neurology</rights><rights>2020 American Academy of Neurology.</rights><rights>2020 American Academy of Neurology 2020 American Academy of Neurology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4053-56e1b3881c6aa042803bc4db903d9d8cc57db209e9c256b78247476a28c7a7073</cites><orcidid>0000-0002-8309-094X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32680943$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baumeister, Sebastian E.</creatorcontrib><creatorcontrib>Karch, André</creatorcontrib><creatorcontrib>Bahls, Martin</creatorcontrib><creatorcontrib>Teumer, Alexander</creatorcontrib><creatorcontrib>Leitzmann, Michael F.</creatorcontrib><creatorcontrib>Baurecht, Hansjörg</creatorcontrib><title>Physical activity and risk of Alzheimer disease: A 2-sample mendelian randomization study</title><title>Neurology</title><addtitle>Neurology</addtitle><description>OBJECTIVEEvidence from observational studies for the effect of physical activity on the risk of Alzheimer disease (AD) is inconclusive. We performed a 2-sample mendelian randomization analysis to examine whether physical activity is protective for AD.
METHODSSummary data of genome-wide association studies on physical activity and AD were used. The primary study population included 21,982 patients with AD and 41,944 cognitively normal controls. Eight single nucleotide polymorphisms (SNPs) known at p < 5 × 10 to be associated with average accelerations and 8 SNPs associated at p < 5 × 10 with vigorous physical activity (fraction of accelerations >425 milligravities) served as instrumental variables.
RESULTSThere was no association between genetically predicted average accelerations with the risk of AD (inverse variance weighted odds ratio [OR] per SD increment1.03, 95% confidence interval 0.97–1.10, p = 0.332). Genetic liability for fraction of accelerations >425 milligravities was unrelated to AD risk.
CONCLUSIONThe present study does not support a causal association between physical activity and risk of AD.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - genetics</subject><subject>Biological Specimen Banks</subject><subject>Case-Control Studies</subject><subject>Exercise</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genome-Wide Association Study - statistics & numerical data</subject><subject>Humans</subject><subject>Male</subject><subject>Mendelian Randomization Analysis</subject><subject>Middle Aged</subject><subject>Null Hypothesis</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Factors</subject><issn>0028-3878</issn><issn>1526-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtKJDEUhoMo2jq-gUheoDS3ysWF0IjOCI3OQplxFVJJ2oqmqpqkuqV9eqtpx9vCOQTOIv_3HfgBOMDoCBNMjv9cTY7Q--Dh0Q0wwiXhBafk7yYYIURkQaWQO2A354chURKhtsEOJVwixegI3P2ulzlYE6GxfViEfglN62AK-RF2UziOz7UPjU_QhexN9idwDEmRTTOLHja-dT4G08I0QF0Tnk0fuhbmfu6WP8DW1MTs91_3Hri9OL85-1VMrn9eno0nhWWopEXJPa6olNhyYxAjEtHKMlcpRJ1y0tpSuIog5ZUlJa-EJEwwwQ2RVhiBBN0Dp2vvbF413lnf9slEPUuhMWmpOxP055821Pq-W2ihOKVMDQK2FtjU5Zz89I3FSK-q1kPV-mvVA3b48e4b9K_bISDXgacu9j7lxzh_8knX3sS-_p-bfYOuchxjVhBEEFJEoWJFSvoCXLKbtQ</recordid><startdate>20200929</startdate><enddate>20200929</enddate><creator>Baumeister, Sebastian E.</creator><creator>Karch, André</creator><creator>Bahls, Martin</creator><creator>Teumer, Alexander</creator><creator>Leitzmann, Michael F.</creator><creator>Baurecht, Hansjörg</creator><general>American Academy of Neurology</general><general>Lippincott Williams & Wilkins</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8309-094X</orcidid></search><sort><creationdate>20200929</creationdate><title>Physical activity and risk of Alzheimer disease: A 2-sample mendelian randomization study</title><author>Baumeister, Sebastian E. ; Karch, André ; Bahls, Martin ; Teumer, Alexander ; Leitzmann, Michael F. ; Baurecht, Hansjörg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4053-56e1b3881c6aa042803bc4db903d9d8cc57db209e9c256b78247476a28c7a7073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - genetics</topic><topic>Biological Specimen Banks</topic><topic>Case-Control Studies</topic><topic>Exercise</topic><topic>Female</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genome-Wide Association Study - statistics & numerical data</topic><topic>Humans</topic><topic>Male</topic><topic>Mendelian Randomization Analysis</topic><topic>Middle Aged</topic><topic>Null Hypothesis</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baumeister, Sebastian E.</creatorcontrib><creatorcontrib>Karch, André</creatorcontrib><creatorcontrib>Bahls, Martin</creatorcontrib><creatorcontrib>Teumer, Alexander</creatorcontrib><creatorcontrib>Leitzmann, Michael F.</creatorcontrib><creatorcontrib>Baurecht, Hansjörg</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baumeister, Sebastian E.</au><au>Karch, André</au><au>Bahls, Martin</au><au>Teumer, Alexander</au><au>Leitzmann, Michael F.</au><au>Baurecht, Hansjörg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Physical activity and risk of Alzheimer disease: A 2-sample mendelian randomization study</atitle><jtitle>Neurology</jtitle><addtitle>Neurology</addtitle><date>2020-09-29</date><risdate>2020</risdate><volume>95</volume><issue>13</issue><spage>e1897</spage><epage>e1905</epage><pages>e1897-e1905</pages><issn>0028-3878</issn><eissn>1526-632X</eissn><abstract>OBJECTIVEEvidence from observational studies for the effect of physical activity on the risk of Alzheimer disease (AD) is inconclusive. We performed a 2-sample mendelian randomization analysis to examine whether physical activity is protective for AD.
METHODSSummary data of genome-wide association studies on physical activity and AD were used. The primary study population included 21,982 patients with AD and 41,944 cognitively normal controls. Eight single nucleotide polymorphisms (SNPs) known at p < 5 × 10 to be associated with average accelerations and 8 SNPs associated at p < 5 × 10 with vigorous physical activity (fraction of accelerations >425 milligravities) served as instrumental variables.
RESULTSThere was no association between genetically predicted average accelerations with the risk of AD (inverse variance weighted odds ratio [OR] per SD increment1.03, 95% confidence interval 0.97–1.10, p = 0.332). Genetic liability for fraction of accelerations >425 milligravities was unrelated to AD risk.
CONCLUSIONThe present study does not support a causal association between physical activity and risk of AD.</abstract><cop>United States</cop><pub>American Academy of Neurology</pub><pmid>32680943</pmid><doi>10.1212/WNL.0000000000010013</doi><orcidid>https://orcid.org/0000-0002-8309-094X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aged, 80 and over Alzheimer Disease - genetics Biological Specimen Banks Case-Control Studies Exercise Female Genetic Predisposition to Disease - genetics Genome-Wide Association Study - statistics & numerical data Humans Male Mendelian Randomization Analysis Middle Aged Null Hypothesis Polymorphism, Single Nucleotide Risk Factors |
| title | Physical activity and risk of Alzheimer disease: A 2-sample mendelian randomization study |
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