Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the r...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Molecular biology reports 2021-03, Vol.48 (3), p.2601-2610
Hauptverfasser: Siokas, Vasileios, Aloizou, Athina-Maria, Liampas, Ioannis, Tsouris, Zisis, Mentis, Alexios-Fotios A., Nasios, Grigorios, Papadimitriou, Dimitra, Bogdanos, Dimitrios P., Hadjigeorgiou, Georgios M., Dardiotis, Efthimios
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 2610
container_issue 3
container_start_page 2601
container_title Molecular biology reports
container_volume 48
creator Siokas, Vasileios
Aloizou, Athina-Maria
Liampas, Ioannis
Tsouris, Zisis
Mentis, Alexios-Fotios A.
Nasios, Grigorios
Papadimitriou, Dimitra
Bogdanos, Dimitrios P.
Hadjigeorgiou, Georgios M.
Dardiotis, Efthimios
description Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the rs75932628 variant in ALS have yielded inconsistent results, so far. To assess the role of TREM2 rs75932628 on ALS risk. We genotyped 155 patients with sporadic ALS and 155 healthy controls for TREM2 rs75932628. We also merged and meta-analyzed our data with data from previous studies (with a total of 7524 ALS cases and 14,675 controls), regarding TREM2 rs75932628 and ALS. No ALS or healthy subjects carried the TREM2 rs75932628-T variant. Results from meta-analyses (overall approach and sensitivity analyses) yielded no significant results for possible connection between TREM2 rs75932628-T variant and ALS. Based on our results, TREM2 rs75932628 does not seem to play a determining role to the pathophysiology of ALS.
doi_str_mv 10.1007/s11033-021-06312-1
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2509610811</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2509610811</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-56b94fe211573f9d66cef69f732969d0eb6f3e357b4ef11f413b2f62eb976b003</originalsourceid><addsrcrecordid>eNp9kMFOHDEMhqOKqizQF-BQReLCZaidZJLJsULQIi2qhIBrlJl1YGB2siSzVLx9s10oUg89-eDPv-2PsUOEEwQwXzMiSFmBwAq0RFHhBzbD2shKWdPssBlIwEo1Ne6yvZwfAEChqT-xXSkbocvMjN3OfffIY-A-59j1furjyFuafhGN_Prq7FLwlE1tpdCi4c8-9X6cuB8X3C9f4pTi6r7v-OAnSn7guRsoxdznA_Yx-CHT59e6z27Oz65Pf1Tzn98vTr_Nq06aeqpq3VoVSODm6mAXWncUtA1GCqvtAqjVQZKsTasoIAaFshVBC2qt0S2A3GfH29xVik9rypNb9rmjYfAjxXV2ogarERrEgh79gz7EdRrLdYUyxiglrSqU2FJd-SMnCm6V-qVPLw7Bbay7rXVXrLs_1t0m-str9Lpd0uLvyJvmAsgtkEtrvKP0vvs_sb8BQJSKgQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2577744394</pqid></control><display><type>article</type><title>Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Siokas, Vasileios ; Aloizou, Athina-Maria ; Liampas, Ioannis ; Tsouris, Zisis ; Mentis, Alexios-Fotios A. ; Nasios, Grigorios ; Papadimitriou, Dimitra ; Bogdanos, Dimitrios P. ; Hadjigeorgiou, Georgios M. ; Dardiotis, Efthimios</creator><creatorcontrib>Siokas, Vasileios ; Aloizou, Athina-Maria ; Liampas, Ioannis ; Tsouris, Zisis ; Mentis, Alexios-Fotios A. ; Nasios, Grigorios ; Papadimitriou, Dimitra ; Bogdanos, Dimitrios P. ; Hadjigeorgiou, Georgios M. ; Dardiotis, Efthimios</creatorcontrib><description>Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the rs75932628 variant in ALS have yielded inconsistent results, so far. To assess the role of TREM2 rs75932628 on ALS risk. We genotyped 155 patients with sporadic ALS and 155 healthy controls for TREM2 rs75932628. We also merged and meta-analyzed our data with data from previous studies (with a total of 7524 ALS cases and 14,675 controls), regarding TREM2 rs75932628 and ALS. No ALS or healthy subjects carried the TREM2 rs75932628-T variant. Results from meta-analyses (overall approach and sensitivity analyses) yielded no significant results for possible connection between TREM2 rs75932628-T variant and ALS. Based on our results, TREM2 rs75932628 does not seem to play a determining role to the pathophysiology of ALS.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-021-06312-1</identifier><identifier>PMID: 33826063</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - genetics ; Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Cohort Studies ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Histology ; Humans ; Life Sciences ; Male ; Membrane Glycoproteins - genetics ; Meta-Analysis as Topic ; Middle Aged ; Morphology ; Neurodegenerative diseases ; Original Article ; Pathogenesis ; Polymorphism, Single Nucleotide - genetics ; Publication Bias ; Receptors, Immunologic - genetics ; Sensitivity analysis</subject><ispartof>Molecular biology reports, 2021-03, Vol.48 (3), p.2601-2610</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-56b94fe211573f9d66cef69f732969d0eb6f3e357b4ef11f413b2f62eb976b003</citedby><cites>FETCH-LOGICAL-c375t-56b94fe211573f9d66cef69f732969d0eb6f3e357b4ef11f413b2f62eb976b003</cites><orcidid>0000-0003-2957-641X</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/s11033-021-06312-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-021-06312-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33826063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Siokas, Vasileios</creatorcontrib><creatorcontrib>Aloizou, Athina-Maria</creatorcontrib><creatorcontrib>Liampas, Ioannis</creatorcontrib><creatorcontrib>Tsouris, Zisis</creatorcontrib><creatorcontrib>Mentis, Alexios-Fotios A.</creatorcontrib><creatorcontrib>Nasios, Grigorios</creatorcontrib><creatorcontrib>Papadimitriou, Dimitra</creatorcontrib><creatorcontrib>Bogdanos, Dimitrios P.</creatorcontrib><creatorcontrib>Hadjigeorgiou, Georgios M.</creatorcontrib><creatorcontrib>Dardiotis, Efthimios</creatorcontrib><title>Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the rs75932628 variant in ALS have yielded inconsistent results, so far. To assess the role of TREM2 rs75932628 on ALS risk. We genotyped 155 patients with sporadic ALS and 155 healthy controls for TREM2 rs75932628. We also merged and meta-analyzed our data with data from previous studies (with a total of 7524 ALS cases and 14,675 controls), regarding TREM2 rs75932628 and ALS. No ALS or healthy subjects carried the TREM2 rs75932628-T variant. Results from meta-analyses (overall approach and sensitivity analyses) yielded no significant results for possible connection between TREM2 rs75932628-T variant and ALS. Based on our results, TREM2 rs75932628 does not seem to play a determining role to the pathophysiology of ALS.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cohort Studies</subject><subject>Female</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Histology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Meta-Analysis as Topic</subject><subject>Middle Aged</subject><subject>Morphology</subject><subject>Neurodegenerative diseases</subject><subject>Original Article</subject><subject>Pathogenesis</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Publication Bias</subject><subject>Receptors, Immunologic - genetics</subject><subject>Sensitivity analysis</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kMFOHDEMhqOKqizQF-BQReLCZaidZJLJsULQIi2qhIBrlJl1YGB2siSzVLx9s10oUg89-eDPv-2PsUOEEwQwXzMiSFmBwAq0RFHhBzbD2shKWdPssBlIwEo1Ne6yvZwfAEChqT-xXSkbocvMjN3OfffIY-A-59j1furjyFuafhGN_Prq7FLwlE1tpdCi4c8-9X6cuB8X3C9f4pTi6r7v-OAnSn7guRsoxdznA_Yx-CHT59e6z27Oz65Pf1Tzn98vTr_Nq06aeqpq3VoVSODm6mAXWncUtA1GCqvtAqjVQZKsTasoIAaFshVBC2qt0S2A3GfH29xVik9rypNb9rmjYfAjxXV2ogarERrEgh79gz7EdRrLdYUyxiglrSqU2FJd-SMnCm6V-qVPLw7Bbay7rXVXrLs_1t0m-str9Lpd0uLvyJvmAsgtkEtrvKP0vvs_sb8BQJSKgQ</recordid><startdate>20210301</startdate><enddate>20210301</enddate><creator>Siokas, Vasileios</creator><creator>Aloizou, Athina-Maria</creator><creator>Liampas, Ioannis</creator><creator>Tsouris, Zisis</creator><creator>Mentis, Alexios-Fotios A.</creator><creator>Nasios, Grigorios</creator><creator>Papadimitriou, Dimitra</creator><creator>Bogdanos, Dimitrios P.</creator><creator>Hadjigeorgiou, Georgios M.</creator><creator>Dardiotis, Efthimios</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2957-641X</orcidid></search><sort><creationdate>20210301</creationdate><title>Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis</title><author>Siokas, Vasileios ; Aloizou, Athina-Maria ; Liampas, Ioannis ; Tsouris, Zisis ; Mentis, Alexios-Fotios A. ; Nasios, Grigorios ; Papadimitriou, Dimitra ; Bogdanos, Dimitrios P. ; Hadjigeorgiou, Georgios M. ; Dardiotis, Efthimios</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-56b94fe211573f9d66cef69f732969d0eb6f3e357b4ef11f413b2f62eb976b003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cohort Studies</topic><topic>Female</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Histology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Meta-Analysis as Topic</topic><topic>Middle Aged</topic><topic>Morphology</topic><topic>Neurodegenerative diseases</topic><topic>Original Article</topic><topic>Pathogenesis</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Publication Bias</topic><topic>Receptors, Immunologic - genetics</topic><topic>Sensitivity analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Siokas, Vasileios</creatorcontrib><creatorcontrib>Aloizou, Athina-Maria</creatorcontrib><creatorcontrib>Liampas, Ioannis</creatorcontrib><creatorcontrib>Tsouris, Zisis</creatorcontrib><creatorcontrib>Mentis, Alexios-Fotios A.</creatorcontrib><creatorcontrib>Nasios, Grigorios</creatorcontrib><creatorcontrib>Papadimitriou, Dimitra</creatorcontrib><creatorcontrib>Bogdanos, Dimitrios P.</creatorcontrib><creatorcontrib>Hadjigeorgiou, Georgios M.</creatorcontrib><creatorcontrib>Dardiotis, Efthimios</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Siokas, Vasileios</au><au>Aloizou, Athina-Maria</au><au>Liampas, Ioannis</au><au>Tsouris, Zisis</au><au>Mentis, Alexios-Fotios A.</au><au>Nasios, Grigorios</au><au>Papadimitriou, Dimitra</au><au>Bogdanos, Dimitrios P.</au><au>Hadjigeorgiou, Georgios M.</au><au>Dardiotis, Efthimios</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>48</volume><issue>3</issue><spage>2601</spage><epage>2610</epage><pages>2601-2610</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the rs75932628 variant in ALS have yielded inconsistent results, so far. To assess the role of TREM2 rs75932628 on ALS risk. We genotyped 155 patients with sporadic ALS and 155 healthy controls for TREM2 rs75932628. We also merged and meta-analyzed our data with data from previous studies (with a total of 7524 ALS cases and 14,675 controls), regarding TREM2 rs75932628 and ALS. No ALS or healthy subjects carried the TREM2 rs75932628-T variant. Results from meta-analyses (overall approach and sensitivity analyses) yielded no significant results for possible connection between TREM2 rs75932628-T variant and ALS. Based on our results, TREM2 rs75932628 does not seem to play a determining role to the pathophysiology of ALS.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>33826063</pmid><doi>10.1007/s11033-021-06312-1</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-2957-641X</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0301-4851
ispartof Molecular biology reports, 2021-03, Vol.48 (3), p.2601-2610
issn 0301-4851
1573-4978
language eng
recordid cdi_proquest_miscellaneous_2509610811
source MEDLINE; SpringerLink Journals - AutoHoldings
subjects Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - genetics
Animal Anatomy
Animal Biochemistry
Biomedical and Life Sciences
Cohort Studies
Female
Genetic Association Studies
Genetic Predisposition to Disease
Histology
Humans
Life Sciences
Male
Membrane Glycoproteins - genetics
Meta-Analysis as Topic
Middle Aged
Morphology
Neurodegenerative diseases
Original Article
Pathogenesis
Polymorphism, Single Nucleotide - genetics
Publication Bias
Receptors, Immunologic - genetics
Sensitivity analysis
title Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T21%3A14%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Lack%20of%20association%20between%20TREM2%20rs75932628%20variant%20and%20amyotrophic%20lateral%20sclerosis&rft.jtitle=Molecular%20biology%20reports&rft.au=Siokas,%20Vasileios&rft.date=2021-03-01&rft.volume=48&rft.issue=3&rft.spage=2601&rft.epage=2610&rft.pages=2601-2610&rft.issn=0301-4851&rft.eissn=1573-4978&rft_id=info:doi/10.1007/s11033-021-06312-1&rft_dat=%3Cproquest_cross%3E2509610811%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2577744394&rft_id=info:pmid/33826063&rfr_iscdi=true