Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease
Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hi...
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description | Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD. |
doi_str_mv | 10.1111/jcmm.13998 |
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Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13998</identifier><identifier>PMID: 30488668</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adhesion ; Aged ; Aged, 80 and over ; Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amyloid ; Amyloid - genetics ; Amyloid - metabolism ; Associative learning ; Associative memory ; Autopsy ; Calcium ; Calcium - metabolism ; Calcium Signaling ; Case-Control Studies ; cell‐adhesion molecules ; Dendrites ; Dentate gyrus ; Disease Progression ; Female ; Gene Expression ; Glycoproteins ; Granule cells ; Hippocampal plasticity ; Hippocampus ; Hippocampus - metabolism ; Hippocampus - pathology ; human hippocampus ; Humans ; immunohistochemistry ; Immunoreactivity ; Learning ; Localization ; Male ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Neurodegeneration ; Neurodegenerative diseases ; Neuronal Plasticity - genetics ; Neurons - metabolism ; Neurons - pathology ; Plasticity ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Pyramidal cells ; Short Communication ; Short Communications ; Subiculum ; Synapses - genetics ; Synapses - metabolism ; Synapses - pathology ; Synaptic plasticity ; Synaptic Transmission - genetics ; Tau protein ; tau Proteins - genetics ; tau Proteins - metabolism ; Tissues</subject><ispartof>JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2019-02, Vol.23 (2), p.1602-1607</ispartof><rights>2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4868-9720890825a369c3bacdb5485dd1e8aabdc55deb66c604df6293e7241c9041163</citedby><cites>FETCH-LOGICAL-c4868-9720890825a369c3bacdb5485dd1e8aabdc55deb66c604df6293e7241c9041163</cites><orcidid>0000-0002-5713-4910</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349345/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349345/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30488668$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:140359615$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Ilic, Katarina</creatorcontrib><creatorcontrib>Mlinac‐Jerkovic, Kristina</creatorcontrib><creatorcontrib>Jovanov‐Milosevic, Natasa</creatorcontrib><creatorcontrib>Simic, Goran</creatorcontrib><creatorcontrib>Habek, Nikola</creatorcontrib><creatorcontrib>Bogdanovic, Nenad</creatorcontrib><creatorcontrib>Kalanj‐Bognar, Svjetlana</creatorcontrib><title>Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease</title><title>JOURNAL OF CELLULAR AND MOLECULAR MEDICINE</title><addtitle>J Cell Mol Med</addtitle><description>Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD.</description><subject>Adhesion</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Amyloid - genetics</subject><subject>Amyloid - metabolism</subject><subject>Associative learning</subject><subject>Associative memory</subject><subject>Autopsy</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling</subject><subject>Case-Control Studies</subject><subject>cell‐adhesion molecules</subject><subject>Dendrites</subject><subject>Dentate gyrus</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Glycoproteins</subject><subject>Granule cells</subject><subject>Hippocampal plasticity</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>human hippocampus</subject><subject>Humans</subject><subject>immunohistochemistry</subject><subject>Immunoreactivity</subject><subject>Learning</subject><subject>Localization</subject><subject>Male</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neuronal Plasticity - genetics</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Plasticity</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Pyramidal cells</subject><subject>Short Communication</subject><subject>Short Communications</subject><subject>Subiculum</subject><subject>Synapses - genetics</subject><subject>Synapses - metabolism</subject><subject>Synapses - pathology</subject><subject>Synaptic plasticity</subject><subject>Synaptic Transmission - genetics</subject><subject>Tau protein</subject><subject>tau Proteins - genetics</subject><subject>tau Proteins - metabolism</subject><subject>Tissues</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>D8T</sourceid><recordid>eNp9kcFu1DAQhi0EoqVw4QFQJA6gSil27Dj2BalaQQtqxQXOlmPPdr04cbATynLiEXhGngSnWSrKAV_smfn8a_T_CD0l-ITk82pruu6EUCnFPXRIalGVTFJ2f_8mgooD9CilLcaUZ-whOqCYCcG5OERw7oYhGN0N2hfwbYiQkgt9EdaFAe9__fip7QZuWld-Z8IQwwiuL3qYYhi8TmMuXCq0HyGCLXJ16r9vwHUQX6TCugQ6wWP0YK19gif7-wh9evvm4-q8vPhw9m51elEaJrgoZVNhIbGoak25NLTVxrY1E7W1BITWrTV1baHl3HDM7JpXkkJTMWIkZoRweoTKRTddwzC1aoiu03GngnZq3_qcX6CYoI2Y-dcLnycdWAP9GLW_8-3upHcbdRW-Kk5ni-ss8HIvEMOXCdKoOpdm43QPYUqqyn7XvJG0yujzf9BtmGKf7chUQ7iopZCZOl4oE0NKEda3yxCs5rTVnLa6STvDz_5e_xb9E28GyAJcOw-7_0ip96vLy0X0N2L7uO0</recordid><startdate>201902</startdate><enddate>201902</enddate><creator>Ilic, Katarina</creator><creator>Mlinac‐Jerkovic, Kristina</creator><creator>Jovanov‐Milosevic, Natasa</creator><creator>Simic, Goran</creator><creator>Habek, Nikola</creator><creator>Bogdanovic, Nenad</creator><creator>Kalanj‐Bognar, Svjetlana</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><orcidid>https://orcid.org/0000-0002-5713-4910</orcidid></search><sort><creationdate>201902</creationdate><title>Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease</title><author>Ilic, Katarina ; Mlinac‐Jerkovic, Kristina ; Jovanov‐Milosevic, Natasa ; Simic, Goran ; Habek, Nikola ; Bogdanovic, Nenad ; Kalanj‐Bognar, Svjetlana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4868-9720890825a369c3bacdb5485dd1e8aabdc55deb66c604df6293e7241c9041163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adhesion</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Amyloid - genetics</topic><topic>Amyloid - metabolism</topic><topic>Associative learning</topic><topic>Associative memory</topic><topic>Autopsy</topic><topic>Calcium</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling</topic><topic>Case-Control Studies</topic><topic>cell‐adhesion molecules</topic><topic>Dendrites</topic><topic>Dentate gyrus</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Glycoproteins</topic><topic>Granule cells</topic><topic>Hippocampal plasticity</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>human hippocampus</topic><topic>Humans</topic><topic>immunohistochemistry</topic><topic>Immunoreactivity</topic><topic>Learning</topic><topic>Localization</topic><topic>Male</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neuronal Plasticity - genetics</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Plasticity</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Pyramidal cells</topic><topic>Short Communication</topic><topic>Short Communications</topic><topic>Subiculum</topic><topic>Synapses - genetics</topic><topic>Synapses - metabolism</topic><topic>Synapses - pathology</topic><topic>Synaptic plasticity</topic><topic>Synaptic Transmission - genetics</topic><topic>Tau protein</topic><topic>tau Proteins - genetics</topic><topic>tau Proteins - metabolism</topic><topic>Tissues</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ilic, Katarina</creatorcontrib><creatorcontrib>Mlinac‐Jerkovic, Kristina</creatorcontrib><creatorcontrib>Jovanov‐Milosevic, Natasa</creatorcontrib><creatorcontrib>Simic, Goran</creatorcontrib><creatorcontrib>Habek, Nikola</creatorcontrib><creatorcontrib>Bogdanovic, Nenad</creatorcontrib><creatorcontrib>Kalanj‐Bognar, Svjetlana</creatorcontrib><collection>Wiley Online Library Open Access</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 Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</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>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 Edition)</collection><collection>ProQuest Central UK/Ireland</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 & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>JOURNAL OF CELLULAR AND MOLECULAR MEDICINE</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ilic, Katarina</au><au>Mlinac‐Jerkovic, Kristina</au><au>Jovanov‐Milosevic, Natasa</au><au>Simic, Goran</au><au>Habek, Nikola</au><au>Bogdanovic, Nenad</au><au>Kalanj‐Bognar, Svjetlana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease</atitle><jtitle>JOURNAL OF CELLULAR AND MOLECULAR MEDICINE</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-02</date><risdate>2019</risdate><volume>23</volume><issue>2</issue><spage>1602</spage><epage>1607</epage><pages>1602-1607</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30488668</pmid><doi>10.1111/jcmm.13998</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-5713-4910</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adhesion Aged Aged, 80 and over Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid Amyloid - genetics Amyloid - metabolism Associative learning Associative memory Autopsy Calcium Calcium - metabolism Calcium Signaling Case-Control Studies cell‐adhesion molecules Dendrites Dentate gyrus Disease Progression Female Gene Expression Glycoproteins Granule cells Hippocampal plasticity Hippocampus Hippocampus - metabolism Hippocampus - pathology human hippocampus Humans immunohistochemistry Immunoreactivity Learning Localization Male Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Neurodegeneration Neurodegenerative diseases Neuronal Plasticity - genetics Neurons - metabolism Neurons - pathology Plasticity Protein Isoforms - genetics Protein Isoforms - metabolism Pyramidal cells Short Communication Short Communications Subiculum Synapses - genetics Synapses - metabolism Synapses - pathology Synaptic plasticity Synaptic Transmission - genetics Tau protein tau Proteins - genetics tau Proteins - metabolism Tissues |
title | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
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