Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study
Background Epidemiological evidence suggests that there is an association between rheumatoid arthritis (RA) and Alzheimer’s disease (AD). However, the causal relationship between RA and AD remains unclear. Therefore, this study aimed to investigate the causal relationship between RA and AD. Methods...
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| Veröffentlicht in: | Inflammopharmacology 2024-02, Vol.32 (1), p.863-871 |
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| container_title | Inflammopharmacology |
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| creator | Li, Guo-Shuai Yang, Yong-Ze Ma, Guo-Rong Li, Peng-Fei Cheng, Qing-Hao Zhang, An-Ren Zhang, Zhuang-Zhuang Zhang, Fu-Kang Yang, Xin Fan, Hua Guo, Hong-Zhang |
| description | Background
Epidemiological evidence suggests that there is an association between rheumatoid arthritis (RA) and Alzheimer’s disease (AD). However, the causal relationship between RA and AD remains unclear. Therefore, this study aimed to investigate the causal relationship between RA and AD.
Methods
Using publicly available genome-wide association study datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using the inverse-variance weighted (IVW), weighted median, MR‒Egger regression, simple mode, and weighted mode methods.
Results
The results of MR for the causal effect of RA on AD (IVW, odds ratio [OR] = 0.959, 95% confidence interval [CI]: 0.941–0.978,
P
= 2.752E-05; weighted median, OR = 0.960, 95% CI: 0.937–0.984,
P
= 0.001) revealed a causal association between genetic susceptibility to RA and an increased risk of AD. The results of MR for the causal effect of AD on RA (IVW, OR = 0.978, 95% CI: 0.906–1.056,
P
= 0.576; weighted median, OR = 0.966, 95% CI: 0.894–1.043,
P
= 0.382) indicated that there was no causal association between genetic susceptibility to AD and an increased risk of RA.
Conclusions
The results of this two-way two-sample Mendelian randomization analysis revealed a causal association between genetic susceptibility to RA and a reduced risk of AD but did not reveal a causal association between genetic susceptibility to AD and an increased or reduced risk of RA. |
| doi_str_mv | 10.1007/s10787-023-01397-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2907196262</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2907196262</sourcerecordid><originalsourceid>FETCH-LOGICAL-c298t-c24ac42c43ce23446d3e3bbf20ae1b2dfe164c11eb56a7001e529de8db5c5ac03</originalsourceid><addsrcrecordid>eNp9kMtuFDEQRS1ERIbAD7BAXrJp8KPt7mYXRbykoEgI1la1XZ1x1I_B5Q5KVkh8Bb-XL8HDJCyRSq6Fz71SHcZeSPFaCtG8ISmatqmE0pWQumsq84htpLFtZaxoH7ON6JSpatupY_aU6EoIYRvbPWHHupVGmrbesF9ftrhOkJcYOKS8TTFH4mWA79KS0ed4jXwAn5fE4RLiTJmfjrdbjBOmu5-_iYdICIRvS6SPIaZ9Zplh5PnHUhFMuxH5Z5wDjhFmnmAOyxRvYQ9xymu4ecaOBhgJn9_vE_bt_buvZx-r84sPn85OzyuvujaXtwZfK19rj0rXtQ0add8PSgDKXoUBpa29lNgbC40QEo3qArahN96AF_qEvTr0lsu-r0jZTZE8jiPMuKzkVCca2VllVUHVAfVpIUo4uF2KE6QbJ4Xby3cH-a7Id3_lO1NCL-_7137C8C_yYLsA-gBQ-ZovMbmrZU1FFf2v9g-fBpRt</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2907196262</pqid></control><display><type>article</type><title>Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study</title><source>SpringerLink Journals (MCLS)</source><creator>Li, Guo-Shuai ; Yang, Yong-Ze ; Ma, Guo-Rong ; Li, Peng-Fei ; Cheng, Qing-Hao ; Zhang, An-Ren ; Zhang, Zhuang-Zhuang ; Zhang, Fu-Kang ; Yang, Xin ; Fan, Hua ; Guo, Hong-Zhang</creator><creatorcontrib>Li, Guo-Shuai ; Yang, Yong-Ze ; Ma, Guo-Rong ; Li, Peng-Fei ; Cheng, Qing-Hao ; Zhang, An-Ren ; Zhang, Zhuang-Zhuang ; Zhang, Fu-Kang ; Yang, Xin ; Fan, Hua ; Guo, Hong-Zhang</creatorcontrib><description>Background
Epidemiological evidence suggests that there is an association between rheumatoid arthritis (RA) and Alzheimer’s disease (AD). However, the causal relationship between RA and AD remains unclear. Therefore, this study aimed to investigate the causal relationship between RA and AD.
Methods
Using publicly available genome-wide association study datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using the inverse-variance weighted (IVW), weighted median, MR‒Egger regression, simple mode, and weighted mode methods.
Results
The results of MR for the causal effect of RA on AD (IVW, odds ratio [OR] = 0.959, 95% confidence interval [CI]: 0.941–0.978,
P
= 2.752E-05; weighted median, OR = 0.960, 95% CI: 0.937–0.984,
P
= 0.001) revealed a causal association between genetic susceptibility to RA and an increased risk of AD. The results of MR for the causal effect of AD on RA (IVW, OR = 0.978, 95% CI: 0.906–1.056,
P
= 0.576; weighted median, OR = 0.966, 95% CI: 0.894–1.043,
P
= 0.382) indicated that there was no causal association between genetic susceptibility to AD and an increased risk of RA.
Conclusions
The results of this two-way two-sample Mendelian randomization analysis revealed a causal association between genetic susceptibility to RA and a reduced risk of AD but did not reveal a causal association between genetic susceptibility to AD and an increased or reduced risk of RA.</description><identifier>ISSN: 0925-4692</identifier><identifier>EISSN: 1568-5608</identifier><identifier>DOI: 10.1007/s10787-023-01397-5</identifier><identifier>PMID: 38151584</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Biomedical and Life Sciences ; Biomedicine ; Dermatology ; Gastroenterology ; Immunology ; Original Article ; Pharmacology/Toxicology ; Rheumatology</subject><ispartof>Inflammopharmacology, 2024-02, Vol.32 (1), p.863-871</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c298t-c24ac42c43ce23446d3e3bbf20ae1b2dfe164c11eb56a7001e529de8db5c5ac03</cites><orcidid>0009-0008-3530-3278</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/s10787-023-01397-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10787-023-01397-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38151584$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Guo-Shuai</creatorcontrib><creatorcontrib>Yang, Yong-Ze</creatorcontrib><creatorcontrib>Ma, Guo-Rong</creatorcontrib><creatorcontrib>Li, Peng-Fei</creatorcontrib><creatorcontrib>Cheng, Qing-Hao</creatorcontrib><creatorcontrib>Zhang, An-Ren</creatorcontrib><creatorcontrib>Zhang, Zhuang-Zhuang</creatorcontrib><creatorcontrib>Zhang, Fu-Kang</creatorcontrib><creatorcontrib>Yang, Xin</creatorcontrib><creatorcontrib>Fan, Hua</creatorcontrib><creatorcontrib>Guo, Hong-Zhang</creatorcontrib><title>Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study</title><title>Inflammopharmacology</title><addtitle>Inflammopharmacol</addtitle><addtitle>Inflammopharmacology</addtitle><description>Background
Epidemiological evidence suggests that there is an association between rheumatoid arthritis (RA) and Alzheimer’s disease (AD). However, the causal relationship between RA and AD remains unclear. Therefore, this study aimed to investigate the causal relationship between RA and AD.
Methods
Using publicly available genome-wide association study datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using the inverse-variance weighted (IVW), weighted median, MR‒Egger regression, simple mode, and weighted mode methods.
Results
The results of MR for the causal effect of RA on AD (IVW, odds ratio [OR] = 0.959, 95% confidence interval [CI]: 0.941–0.978,
P
= 2.752E-05; weighted median, OR = 0.960, 95% CI: 0.937–0.984,
P
= 0.001) revealed a causal association between genetic susceptibility to RA and an increased risk of AD. The results of MR for the causal effect of AD on RA (IVW, OR = 0.978, 95% CI: 0.906–1.056,
P
= 0.576; weighted median, OR = 0.966, 95% CI: 0.894–1.043,
P
= 0.382) indicated that there was no causal association between genetic susceptibility to AD and an increased risk of RA.
Conclusions
The results of this two-way two-sample Mendelian randomization analysis revealed a causal association between genetic susceptibility to RA and a reduced risk of AD but did not reveal a causal association between genetic susceptibility to AD and an increased or reduced risk of RA.</description><subject>Allergology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Dermatology</subject><subject>Gastroenterology</subject><subject>Immunology</subject><subject>Original Article</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><issn>0925-4692</issn><issn>1568-5608</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kMtuFDEQRS1ERIbAD7BAXrJp8KPt7mYXRbykoEgI1la1XZ1x1I_B5Q5KVkh8Bb-XL8HDJCyRSq6Fz71SHcZeSPFaCtG8ISmatqmE0pWQumsq84htpLFtZaxoH7ON6JSpatupY_aU6EoIYRvbPWHHupVGmrbesF9ftrhOkJcYOKS8TTFH4mWA79KS0ed4jXwAn5fE4RLiTJmfjrdbjBOmu5-_iYdICIRvS6SPIaZ9Zplh5PnHUhFMuxH5Z5wDjhFmnmAOyxRvYQ9xymu4ecaOBhgJn9_vE_bt_buvZx-r84sPn85OzyuvujaXtwZfK19rj0rXtQ0add8PSgDKXoUBpa29lNgbC40QEo3qArahN96AF_qEvTr0lsu-r0jZTZE8jiPMuKzkVCca2VllVUHVAfVpIUo4uF2KE6QbJ4Xby3cH-a7Id3_lO1NCL-_7137C8C_yYLsA-gBQ-ZovMbmrZU1FFf2v9g-fBpRt</recordid><startdate>20240201</startdate><enddate>20240201</enddate><creator>Li, Guo-Shuai</creator><creator>Yang, Yong-Ze</creator><creator>Ma, Guo-Rong</creator><creator>Li, Peng-Fei</creator><creator>Cheng, Qing-Hao</creator><creator>Zhang, An-Ren</creator><creator>Zhang, Zhuang-Zhuang</creator><creator>Zhang, Fu-Kang</creator><creator>Yang, Xin</creator><creator>Fan, Hua</creator><creator>Guo, Hong-Zhang</creator><general>Springer International Publishing</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0008-3530-3278</orcidid></search><sort><creationdate>20240201</creationdate><title>Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study</title><author>Li, Guo-Shuai ; Yang, Yong-Ze ; Ma, Guo-Rong ; Li, Peng-Fei ; Cheng, Qing-Hao ; Zhang, An-Ren ; Zhang, Zhuang-Zhuang ; Zhang, Fu-Kang ; Yang, Xin ; Fan, Hua ; Guo, Hong-Zhang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c298t-c24ac42c43ce23446d3e3bbf20ae1b2dfe164c11eb56a7001e529de8db5c5ac03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Allergology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Dermatology</topic><topic>Gastroenterology</topic><topic>Immunology</topic><topic>Original Article</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Guo-Shuai</creatorcontrib><creatorcontrib>Yang, Yong-Ze</creatorcontrib><creatorcontrib>Ma, Guo-Rong</creatorcontrib><creatorcontrib>Li, Peng-Fei</creatorcontrib><creatorcontrib>Cheng, Qing-Hao</creatorcontrib><creatorcontrib>Zhang, An-Ren</creatorcontrib><creatorcontrib>Zhang, Zhuang-Zhuang</creatorcontrib><creatorcontrib>Zhang, Fu-Kang</creatorcontrib><creatorcontrib>Yang, Xin</creatorcontrib><creatorcontrib>Fan, Hua</creatorcontrib><creatorcontrib>Guo, Hong-Zhang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Guo-Shuai</au><au>Yang, Yong-Ze</au><au>Ma, Guo-Rong</au><au>Li, Peng-Fei</au><au>Cheng, Qing-Hao</au><au>Zhang, An-Ren</au><au>Zhang, Zhuang-Zhuang</au><au>Zhang, Fu-Kang</au><au>Yang, Xin</au><au>Fan, Hua</au><au>Guo, Hong-Zhang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study</atitle><jtitle>Inflammopharmacology</jtitle><stitle>Inflammopharmacol</stitle><addtitle>Inflammopharmacology</addtitle><date>2024-02-01</date><risdate>2024</risdate><volume>32</volume><issue>1</issue><spage>863</spage><epage>871</epage><pages>863-871</pages><issn>0925-4692</issn><eissn>1568-5608</eissn><abstract>Background
Epidemiological evidence suggests that there is an association between rheumatoid arthritis (RA) and Alzheimer’s disease (AD). However, the causal relationship between RA and AD remains unclear. Therefore, this study aimed to investigate the causal relationship between RA and AD.
Methods
Using publicly available genome-wide association study datasets, bidirectional two-sample Mendelian randomization (TSMR) was performed using the inverse-variance weighted (IVW), weighted median, MR‒Egger regression, simple mode, and weighted mode methods.
Results
The results of MR for the causal effect of RA on AD (IVW, odds ratio [OR] = 0.959, 95% confidence interval [CI]: 0.941–0.978,
P
= 2.752E-05; weighted median, OR = 0.960, 95% CI: 0.937–0.984,
P
= 0.001) revealed a causal association between genetic susceptibility to RA and an increased risk of AD. The results of MR for the causal effect of AD on RA (IVW, OR = 0.978, 95% CI: 0.906–1.056,
P
= 0.576; weighted median, OR = 0.966, 95% CI: 0.894–1.043,
P
= 0.382) indicated that there was no causal association between genetic susceptibility to AD and an increased risk of RA.
Conclusions
The results of this two-way two-sample Mendelian randomization analysis revealed a causal association between genetic susceptibility to RA and a reduced risk of AD but did not reveal a causal association between genetic susceptibility to AD and an increased or reduced risk of RA.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>38151584</pmid><doi>10.1007/s10787-023-01397-5</doi><tpages>9</tpages><orcidid>https://orcid.org/0009-0008-3530-3278</orcidid></addata></record> |
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| subjects | Allergology Biomedical and Life Sciences Biomedicine Dermatology Gastroenterology Immunology Original Article Pharmacology/Toxicology Rheumatology |
| title | Rheumatoid arthritis is a protective factor against Alzheimer’s disease: a bidirectional two-sample Mendelian randomization study |
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