Genetic Association between PLTP Gene Polymorphisms and Alzheimer’s Disease in a Japanese Population
Background/Aims: A recent paper reported that the phospholipid transfer protein (PLTP) reduces phosphorylation of tau in human neuronal cells. In addition, patients with Alzheimer’s disease (AD) have significantly higher levels of PLTP in brain tissue and significantly lower PLTP-mediated phospholip...
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| Veröffentlicht in: | Dementia and geriatric cognitive disorders 2010-08, Vol.30 (1), p.78-82 |
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| creator | Kuerban, Bolati Shibata, Nobuto Komatsu, Miwa Ohnuma, Tohru Arai, Heii |
| description | Background/Aims: A recent paper reported that the phospholipid transfer protein (PLTP) reduces phosphorylation of tau in human neuronal cells. In addition, patients with Alzheimer’s disease (AD) have significantly higher levels of PLTP in brain tissue and significantly lower PLTP-mediated phospholipid transfer activity in cerebrospinal fluid. PLTP also affects apolipoprotein E (APOE) secretion from glial cells. This study aimed to investigate whether single nucleotide polymorphisms (SNPs) of the PLTP gene are associated with AD. Methods: Five SNPs, genotyped using TaqMan® technology, were analyzed using a case-control study design. Furthermore, we also checked for a synergetic association between the PLTP gene, APOE and AD. Our case-control dataset consisted of 180 AD patients and 130 age-matched controls. Results: None of the SNPs showed a statistically significant association. We could not confirm any synergetic association between the SNPs and APOE in our AD patients. Conclusion: Our results indicate that there is no genetic association between PLTP and AD. Due to the relatively small sample size and the incomplete coverage of the region surrounding the PLTP gene of this study, larger genetic studies covering the entire PLTP gene region are needed. |
| doi_str_mv | 10.1159/000318855 |
| format | Article |
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In addition, patients with Alzheimer’s disease (AD) have significantly higher levels of PLTP in brain tissue and significantly lower PLTP-mediated phospholipid transfer activity in cerebrospinal fluid. PLTP also affects apolipoprotein E (APOE) secretion from glial cells. This study aimed to investigate whether single nucleotide polymorphisms (SNPs) of the PLTP gene are associated with AD. Methods: Five SNPs, genotyped using TaqMan® technology, were analyzed using a case-control study design. Furthermore, we also checked for a synergetic association between the PLTP gene, APOE and AD. Our case-control dataset consisted of 180 AD patients and 130 age-matched controls. Results: None of the SNPs showed a statistically significant association. We could not confirm any synergetic association between the SNPs and APOE in our AD patients. Conclusion: Our results indicate that there is no genetic association between PLTP and AD. Due to the relatively small sample size and the incomplete coverage of the region surrounding the PLTP gene of this study, larger genetic studies covering the entire PLTP gene region are needed.</description><identifier>ISSN: 1420-8008</identifier><identifier>EISSN: 1421-9824</identifier><identifier>DOI: 10.1159/000318855</identifier><identifier>PMID: 20714154</identifier><identifier>CODEN: DGCDFX</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer Disease - epidemiology ; Alzheimer Disease - genetics ; Amyloidosis ; Apolipoproteins E - genetics ; Biological and medical sciences ; Case-Control Studies ; Databases, Genetic ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA - genetics ; Female ; Gene Frequency ; Humans ; Japan - epidemiology ; Male ; Medical sciences ; Metabolic diseases ; Middle Aged ; Neurology ; Original Research Article ; Other metabolic disorders ; Phospholipid Transfer Proteins - cerebrospinal fluid ; Phospholipid Transfer Proteins - genetics ; Polymorphism, Genetic - genetics ; Polymorphism, Single Nucleotide ; Regression Analysis ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>Dementia and geriatric cognitive disorders, 2010-08, Vol.30 (1), p.78-82</ispartof><rights>2010 S. Karger AG, Basel</rights><rights>2015 INIST-CNRS</rights><rights>Copyright 2010 S. Karger AG, Basel.</rights><rights>Copyright (c) 2010 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-f51eb22995516a01f388824d23a7ecb4efb73ad914ec5f15c7e18b41ccc6b0683</citedby><cites>FETCH-LOGICAL-c394t-f51eb22995516a01f388824d23a7ecb4efb73ad914ec5f15c7e18b41ccc6b0683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23222516$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20714154$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuerban, Bolati</creatorcontrib><creatorcontrib>Shibata, Nobuto</creatorcontrib><creatorcontrib>Komatsu, Miwa</creatorcontrib><creatorcontrib>Ohnuma, Tohru</creatorcontrib><creatorcontrib>Arai, Heii</creatorcontrib><title>Genetic Association between PLTP Gene Polymorphisms and Alzheimer’s Disease in a Japanese Population</title><title>Dementia and geriatric cognitive disorders</title><addtitle>Dement Geriatr Cogn Disord</addtitle><description>Background/Aims: A recent paper reported that the phospholipid transfer protein (PLTP) reduces phosphorylation of tau in human neuronal cells. In addition, patients with Alzheimer’s disease (AD) have significantly higher levels of PLTP in brain tissue and significantly lower PLTP-mediated phospholipid transfer activity in cerebrospinal fluid. PLTP also affects apolipoprotein E (APOE) secretion from glial cells. This study aimed to investigate whether single nucleotide polymorphisms (SNPs) of the PLTP gene are associated with AD. Methods: Five SNPs, genotyped using TaqMan® technology, were analyzed using a case-control study design. Furthermore, we also checked for a synergetic association between the PLTP gene, APOE and AD. Our case-control dataset consisted of 180 AD patients and 130 age-matched controls. Results: None of the SNPs showed a statistically significant association. We could not confirm any synergetic association between the SNPs and APOE in our AD patients. Conclusion: Our results indicate that there is no genetic association between PLTP and AD. Due to the relatively small sample size and the incomplete coverage of the region surrounding the PLTP gene of this study, larger genetic studies covering the entire PLTP gene region are needed.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer Disease - genetics</subject><subject>Amyloidosis</subject><subject>Apolipoproteins E - genetics</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Databases, Genetic</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA - genetics</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Humans</subject><subject>Japan - epidemiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Original Research Article</subject><subject>Other metabolic disorders</subject><subject>Phospholipid Transfer Proteins - cerebrospinal fluid</subject><subject>Phospholipid Transfer Proteins - genetics</subject><subject>Polymorphism, Genetic - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Regression Analysis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>1420-8008</issn><issn>1421-9824</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqN0TtvFDEQB3ALgcgDCnqELKQIUSx4_Li1y1OAADqJK0K98vpmicO-4tkVChVfg6_HJ8GXOw6JisZ28fPYM3_GnoB4BWDcayGEAmuNuceOQUsonJX6_t1ZFFYIe8ROiK4zK83CPWRHUpSgwehj1lxgj1MMfEk0hOinOPS8xukbYs_Xq8s13wK-HtrbbkjjVaSOuO83fNl-v8LYYfr14yfxN5HQE_LYc88_-tH3SNtb49zelXzEHjS-JXy830_Z53dvL8_fF6tPFx_Ol6siKKenojGAtZTOGQMLL6BR1uZWNlL5EkOtsalL5TcONAbTgAklgq01hBAWtVhYdcpe7OqOabiZkaaqixSwbfOHhpkqZ7SxIP9DlkYLcMqqLJ__I6-HOfW5jYxMHnFeM3q5QyENRAmbakyx8-m2AlFtQ6oOIWX7bF9wrjvcHOSfVDI42wNPwbdN8n2I9NcpKWUeUHZPd-6rT18wHcD-nd_kiaGw</recordid><startdate>201008</startdate><enddate>201008</enddate><creator>Kuerban, Bolati</creator><creator>Shibata, Nobuto</creator><creator>Komatsu, Miwa</creator><creator>Ohnuma, Tohru</creator><creator>Arai, Heii</creator><general>Karger</general><general>S. 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Leukodystrophies. Prion diseases</topic><topic>DNA - genetics</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Humans</topic><topic>Japan - epidemiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Original Research Article</topic><topic>Other metabolic disorders</topic><topic>Phospholipid Transfer Proteins - cerebrospinal fluid</topic><topic>Phospholipid Transfer Proteins - genetics</topic><topic>Polymorphism, Genetic - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Regression Analysis</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuerban, Bolati</creatorcontrib><creatorcontrib>Shibata, Nobuto</creatorcontrib><creatorcontrib>Komatsu, Miwa</creatorcontrib><creatorcontrib>Ohnuma, Tohru</creatorcontrib><creatorcontrib>Arai, Heii</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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 & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Social Science Database</collection><collection>Nursing & Allied Health Premium</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Dementia and geriatric cognitive disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuerban, Bolati</au><au>Shibata, Nobuto</au><au>Komatsu, Miwa</au><au>Ohnuma, Tohru</au><au>Arai, Heii</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic Association between PLTP Gene Polymorphisms and Alzheimer’s Disease in a Japanese Population</atitle><jtitle>Dementia and geriatric cognitive disorders</jtitle><addtitle>Dement Geriatr Cogn Disord</addtitle><date>2010-08</date><risdate>2010</risdate><volume>30</volume><issue>1</issue><spage>78</spage><epage>82</epage><pages>78-82</pages><issn>1420-8008</issn><eissn>1421-9824</eissn><coden>DGCDFX</coden><abstract>Background/Aims: A recent paper reported that the phospholipid transfer protein (PLTP) reduces phosphorylation of tau in human neuronal cells. In addition, patients with Alzheimer’s disease (AD) have significantly higher levels of PLTP in brain tissue and significantly lower PLTP-mediated phospholipid transfer activity in cerebrospinal fluid. PLTP also affects apolipoprotein E (APOE) secretion from glial cells. This study aimed to investigate whether single nucleotide polymorphisms (SNPs) of the PLTP gene are associated with AD. Methods: Five SNPs, genotyped using TaqMan® technology, were analyzed using a case-control study design. Furthermore, we also checked for a synergetic association between the PLTP gene, APOE and AD. Our case-control dataset consisted of 180 AD patients and 130 age-matched controls. Results: None of the SNPs showed a statistically significant association. We could not confirm any synergetic association between the SNPs and APOE in our AD patients. Conclusion: Our results indicate that there is no genetic association between PLTP and AD. Due to the relatively small sample size and the incomplete coverage of the region surrounding the PLTP gene of this study, larger genetic studies covering the entire PLTP gene region are needed.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>20714154</pmid><doi>10.1159/000318855</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - epidemiology Alzheimer Disease - genetics Amyloidosis Apolipoproteins E - genetics Biological and medical sciences Case-Control Studies Databases, Genetic Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA - genetics Female Gene Frequency Humans Japan - epidemiology Male Medical sciences Metabolic diseases Middle Aged Neurology Original Research Article Other metabolic disorders Phospholipid Transfer Proteins - cerebrospinal fluid Phospholipid Transfer Proteins - genetics Polymorphism, Genetic - genetics Polymorphism, Single Nucleotide Regression Analysis Reverse Transcriptase Polymerase Chain Reaction |
| title | Genetic Association between PLTP Gene Polymorphisms and Alzheimer’s Disease in a Japanese Population |
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