Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model
Alzheimer's disease (AD) differs from other forms of dementia in its relation to amyloid β peptide (Aβ). Aβ, a proteolytic product of amyloid precursor proteins (APP), has a toxic effect on neuronal cells, which involves perturbation of their Ca2+ homeostasis. This effect implies that changes o...
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creator | Yamaguchi, Mami Kokai, Yasuo Imai, Shin-Ichi Utsumi, Kumiko Matsumoto, Kyoichi Honda, Hirohito Mizue, Yuka Momma, Masako Maeda, Tetsu Toyomasu, Shozo Ito, Yoichi M. Kobayashi, Seijyu Hashimoto, Eri Saito, Toshikazu Sohma, Hitoshi |
description | Alzheimer's disease (AD) differs from other forms of dementia in its relation to amyloid β peptide (Aβ). Aβ, a proteolytic product of amyloid precursor proteins (APP), has a toxic effect on neuronal cells, which involves perturbation of their Ca2+ homeostasis. This effect implies that changes of protein expression in neuronal cells with calcium stress should provide a molecular marker for this disease. In the present study, we used the supernatant from a neuronal cell culture after incubation with or without Aβ and isolated a Ca2+‐dependent acidic phospholipid binding fraction to perform a proteomic study. Several unique proteins were identified after incubation with Aβ. We focused on annexin A5, among these proteins, because it binds both Ca2+ and lipids likely to be involved in calcium homeostasis. Tg2576 transgenic mice (AD model) overexpressing mutant human APP showed a significant increase of annexin A5 in the brain cortex but not in other organs, including liver, kidney, lung, and intestine. In human plasma samples, the level of annexin A5 was significantly increased in a proportion of AD patients compared with a control group (P < 0.0001 in the logistic regression analysis). From the receiver operating characteristic (ROC) curve with plasma annexin A5 concentrations, the mean area under the curve (AUC 0.898) suggests that annexin A5 is a favorable marker for AD. © 2010 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/jnr.22427 |
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Aβ, a proteolytic product of amyloid precursor proteins (APP), has a toxic effect on neuronal cells, which involves perturbation of their Ca2+ homeostasis. This effect implies that changes of protein expression in neuronal cells with calcium stress should provide a molecular marker for this disease. In the present study, we used the supernatant from a neuronal cell culture after incubation with or without Aβ and isolated a Ca2+‐dependent acidic phospholipid binding fraction to perform a proteomic study. Several unique proteins were identified after incubation with Aβ. We focused on annexin A5, among these proteins, because it binds both Ca2+ and lipids likely to be involved in calcium homeostasis. Tg2576 transgenic mice (AD model) overexpressing mutant human APP showed a significant increase of annexin A5 in the brain cortex but not in other organs, including liver, kidney, lung, and intestine. In human plasma samples, the level of annexin A5 was significantly increased in a proportion of AD patients compared with a control group (P < 0.0001 in the logistic regression analysis). From the receiver operating characteristic (ROC) curve with plasma annexin A5 concentrations, the mean area under the curve (AUC 0.898) suggests that annexin A5 is a favorable marker for AD. © 2010 Wiley‐Liss, Inc.</description><identifier>ISSN: 0360-4012</identifier><identifier>ISSN: 1097-4547</identifier><identifier>EISSN: 1097-4547</identifier><identifier>DOI: 10.1002/jnr.22427</identifier><identifier>PMID: 20648654</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer Disease - blood ; Alzheimer Disease - diagnosis ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid beta-Protein Precursor - biosynthesis ; Amyloid beta-Protein Precursor - genetics ; Amyloid beta-Protein Precursor - physiology ; Animals ; annexin A5 ; Annexin A5 - biosynthesis ; Annexin A5 - blood ; biomarker ; Biomarkers - blood ; Ca2+ stress ; Calcium Signaling - physiology ; Cell Culture Techniques - methods ; Cells, Cultured ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Disease Models, Animal ; Female ; Gene Expression Regulation - physiology ; Homeostasis - genetics ; Homeostasis - physiology ; Humans ; Male ; Mice ; Mice, Inbred ICR ; Mice, Transgenic ; Neurons - cytology ; Neurons - metabolism ; Neurons - pathology ; Organ Specificity - genetics ; Organ Specificity - physiology</subject><ispartof>Journal of neuroscience research, 2010-09, Vol.88 (12), p.2682-2692</ispartof><rights>Copyright © 2010 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4927-2ca4b1e086d5a8216c7ac294f0654e73cc8631160f1959fb0f8788c814dfa4b13</citedby><cites>FETCH-LOGICAL-c4927-2ca4b1e086d5a8216c7ac294f0654e73cc8631160f1959fb0f8788c814dfa4b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjnr.22427$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjnr.22427$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20648654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamaguchi, Mami</creatorcontrib><creatorcontrib>Kokai, Yasuo</creatorcontrib><creatorcontrib>Imai, Shin-Ichi</creatorcontrib><creatorcontrib>Utsumi, Kumiko</creatorcontrib><creatorcontrib>Matsumoto, Kyoichi</creatorcontrib><creatorcontrib>Honda, Hirohito</creatorcontrib><creatorcontrib>Mizue, Yuka</creatorcontrib><creatorcontrib>Momma, Masako</creatorcontrib><creatorcontrib>Maeda, Tetsu</creatorcontrib><creatorcontrib>Toyomasu, Shozo</creatorcontrib><creatorcontrib>Ito, Yoichi M.</creatorcontrib><creatorcontrib>Kobayashi, Seijyu</creatorcontrib><creatorcontrib>Hashimoto, Eri</creatorcontrib><creatorcontrib>Saito, Toshikazu</creatorcontrib><creatorcontrib>Sohma, Hitoshi</creatorcontrib><title>Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model</title><title>Journal of neuroscience research</title><addtitle>J. Neurosci. Res</addtitle><description>Alzheimer's disease (AD) differs from other forms of dementia in its relation to amyloid β peptide (Aβ). Aβ, a proteolytic product of amyloid precursor proteins (APP), has a toxic effect on neuronal cells, which involves perturbation of their Ca2+ homeostasis. This effect implies that changes of protein expression in neuronal cells with calcium stress should provide a molecular marker for this disease. In the present study, we used the supernatant from a neuronal cell culture after incubation with or without Aβ and isolated a Ca2+‐dependent acidic phospholipid binding fraction to perform a proteomic study. Several unique proteins were identified after incubation with Aβ. We focused on annexin A5, among these proteins, because it binds both Ca2+ and lipids likely to be involved in calcium homeostasis. Tg2576 transgenic mice (AD model) overexpressing mutant human APP showed a significant increase of annexin A5 in the brain cortex but not in other organs, including liver, kidney, lung, and intestine. In human plasma samples, the level of annexin A5 was significantly increased in a proportion of AD patients compared with a control group (P < 0.0001 in the logistic regression analysis). From the receiver operating characteristic (ROC) curve with plasma annexin A5 concentrations, the mean area under the curve (AUC 0.898) suggests that annexin A5 is a favorable marker for AD. © 2010 Wiley‐Liss, Inc.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - blood</subject><subject>Alzheimer Disease - diagnosis</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Protein Precursor - biosynthesis</subject><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Amyloid beta-Protein Precursor - physiology</subject><subject>Animals</subject><subject>annexin A5</subject><subject>Annexin A5 - biosynthesis</subject><subject>Annexin A5 - blood</subject><subject>biomarker</subject><subject>Biomarkers - blood</subject><subject>Ca2+ stress</subject><subject>Calcium Signaling - physiology</subject><subject>Cell Culture Techniques - methods</subject><subject>Cells, Cultured</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gene Expression Regulation - physiology</subject><subject>Homeostasis - genetics</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Mice, Transgenic</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Organ Specificity - genetics</subject><subject>Organ Specificity - physiology</subject><issn>0360-4012</issn><issn>1097-4547</issn><issn>1097-4547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9PFTEUxRujkSe68AuY7oiLgf5vZ_lCFCGI0WBw1_R1brE400L7RsFPb58P2Bk3925-5-TcexB6Tck-JYQdXKWyz5hg-glaUNLrTkihn6IF4Yp0glC2g17UekUI6XvJn6MdRpQwSooFSsfpJ9R1vHTrmBPOAbuU4DYmvJTYVezwKubJlR9QcMgFL8ff3yFOUPYqHmIFVwHPNaZLnGAuObkRexjbmMf1XKC5DXjKc6OmPMD4Ej0Lbqzw6n7voq_v350ffuhOPx0dHy5POy96pjvmnVhRIEYN0hlGldfOs14E0kKD5t4bxSlVJNBe9mFFgtHGeEPFEDZKvov2tr7XJd_M7UA7xboJ5hK0NNYYTmjPufg_qXpphBG6kW-3pC-51gLBXpfYXnNnKbGbHmzrwf7tobFv7l3n1QTDI_nw-AYcbIFfcYS7fzvZk7MvD5bdVhHrGm4fFa0aqzTX0l6cHdnPSn6U3y5O7Dn_A7fuoO0</recordid><startdate>201009</startdate><enddate>201009</enddate><creator>Yamaguchi, Mami</creator><creator>Kokai, Yasuo</creator><creator>Imai, Shin-Ichi</creator><creator>Utsumi, Kumiko</creator><creator>Matsumoto, Kyoichi</creator><creator>Honda, Hirohito</creator><creator>Mizue, Yuka</creator><creator>Momma, Masako</creator><creator>Maeda, Tetsu</creator><creator>Toyomasu, Shozo</creator><creator>Ito, Yoichi M.</creator><creator>Kobayashi, Seijyu</creator><creator>Hashimoto, Eri</creator><creator>Saito, Toshikazu</creator><creator>Sohma, Hitoshi</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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>7TK</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>201009</creationdate><title>Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model</title><author>Yamaguchi, Mami ; Kokai, Yasuo ; Imai, Shin-Ichi ; Utsumi, Kumiko ; Matsumoto, Kyoichi ; Honda, Hirohito ; Mizue, Yuka ; Momma, Masako ; Maeda, Tetsu ; Toyomasu, Shozo ; Ito, Yoichi M. ; Kobayashi, Seijyu ; Hashimoto, Eri ; Saito, Toshikazu ; Sohma, Hitoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4927-2ca4b1e086d5a8216c7ac294f0654e73cc8631160f1959fb0f8788c814dfa4b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - blood</topic><topic>Alzheimer Disease - diagnosis</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Protein Precursor - biosynthesis</topic><topic>Amyloid beta-Protein Precursor - genetics</topic><topic>Amyloid beta-Protein Precursor - physiology</topic><topic>Animals</topic><topic>annexin A5</topic><topic>Annexin A5 - biosynthesis</topic><topic>Annexin A5 - blood</topic><topic>biomarker</topic><topic>Biomarkers - blood</topic><topic>Ca2+ stress</topic><topic>Calcium Signaling - physiology</topic><topic>Cell Culture Techniques - methods</topic><topic>Cells, Cultured</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gene Expression Regulation - physiology</topic><topic>Homeostasis - genetics</topic><topic>Homeostasis - physiology</topic><topic>Humans</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Mice, Transgenic</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Organ Specificity - genetics</topic><topic>Organ Specificity - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamaguchi, Mami</creatorcontrib><creatorcontrib>Kokai, Yasuo</creatorcontrib><creatorcontrib>Imai, Shin-Ichi</creatorcontrib><creatorcontrib>Utsumi, Kumiko</creatorcontrib><creatorcontrib>Matsumoto, Kyoichi</creatorcontrib><creatorcontrib>Honda, Hirohito</creatorcontrib><creatorcontrib>Mizue, Yuka</creatorcontrib><creatorcontrib>Momma, Masako</creatorcontrib><creatorcontrib>Maeda, Tetsu</creatorcontrib><creatorcontrib>Toyomasu, Shozo</creatorcontrib><creatorcontrib>Ito, Yoichi M.</creatorcontrib><creatorcontrib>Kobayashi, Seijyu</creatorcontrib><creatorcontrib>Hashimoto, Eri</creatorcontrib><creatorcontrib>Saito, Toshikazu</creatorcontrib><creatorcontrib>Sohma, Hitoshi</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamaguchi, Mami</au><au>Kokai, Yasuo</au><au>Imai, Shin-Ichi</au><au>Utsumi, Kumiko</au><au>Matsumoto, Kyoichi</au><au>Honda, Hirohito</au><au>Mizue, Yuka</au><au>Momma, Masako</au><au>Maeda, Tetsu</au><au>Toyomasu, Shozo</au><au>Ito, Yoichi M.</au><au>Kobayashi, Seijyu</au><au>Hashimoto, Eri</au><au>Saito, Toshikazu</au><au>Sohma, Hitoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model</atitle><jtitle>Journal of neuroscience research</jtitle><addtitle>J. Neurosci. Res</addtitle><date>2010-09</date><risdate>2010</risdate><volume>88</volume><issue>12</issue><spage>2682</spage><epage>2692</epage><pages>2682-2692</pages><issn>0360-4012</issn><issn>1097-4547</issn><eissn>1097-4547</eissn><abstract>Alzheimer's disease (AD) differs from other forms of dementia in its relation to amyloid β peptide (Aβ). Aβ, a proteolytic product of amyloid precursor proteins (APP), has a toxic effect on neuronal cells, which involves perturbation of their Ca2+ homeostasis. This effect implies that changes of protein expression in neuronal cells with calcium stress should provide a molecular marker for this disease. In the present study, we used the supernatant from a neuronal cell culture after incubation with or without Aβ and isolated a Ca2+‐dependent acidic phospholipid binding fraction to perform a proteomic study. Several unique proteins were identified after incubation with Aβ. We focused on annexin A5, among these proteins, because it binds both Ca2+ and lipids likely to be involved in calcium homeostasis. Tg2576 transgenic mice (AD model) overexpressing mutant human APP showed a significant increase of annexin A5 in the brain cortex but not in other organs, including liver, kidney, lung, and intestine. In human plasma samples, the level of annexin A5 was significantly increased in a proportion of AD patients compared with a control group (P < 0.0001 in the logistic regression analysis). From the receiver operating characteristic (ROC) curve with plasma annexin A5 concentrations, the mean area under the curve (AUC 0.898) suggests that annexin A5 is a favorable marker for AD. © 2010 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20648654</pmid><doi>10.1002/jnr.22427</doi><tpages>11</tpages></addata></record> |
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subjects | Aged Aged, 80 and over Alzheimer Disease - blood Alzheimer Disease - diagnosis Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Protein Precursor - biosynthesis Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - physiology Animals annexin A5 Annexin A5 - biosynthesis Annexin A5 - blood biomarker Biomarkers - blood Ca2+ stress Calcium Signaling - physiology Cell Culture Techniques - methods Cells, Cultured Cerebral Cortex - metabolism Cerebral Cortex - pathology Disease Models, Animal Female Gene Expression Regulation - physiology Homeostasis - genetics Homeostasis - physiology Humans Male Mice Mice, Inbred ICR Mice, Transgenic Neurons - cytology Neurons - metabolism Neurons - pathology Organ Specificity - genetics Organ Specificity - physiology |
title | Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model |
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