Increased S100β neurotrophic activity in Alzheimer's disease temporal lobe
The confirming diagnosis of Alzheimer's disease includes an assessment of the concentration of neuritic plaques in the temporal lobe of the brain. The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of a...
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Veröffentlicht in: | Neurobiology of aging 1992, Vol.13 (1), p.1-7 |
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description | The confirming diagnosis of Alzheimer's disease includes an assessment of the concentration of neuritic plaques in the temporal lobe of the brain. The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of aggregates of overgrown neurites in the neuritic plaques of Alzheimer's disease. The protein S100β, a neurotrophic factor produced by astroglia in the brain, induces neurite outgrowth in cerebral cortical neurons. The generation of specific S100β antibodies, the cloning of a full-length cDNA encoding the S100β mRNA, and the development of a neurite extension assay system for S100β allowed testing of the hypothesis that Alzheimer's disease S100β expression is elevated in brain temporal lobe where neuritic plaques are concentrated. The levels of S100β protein, mRNA, and specific neurotrophic activity were elevated 10–20-fold in extracts of temporal lobe from autopsy samples of Alzheimer's disease patients compared to those of aged control patients. The cells containing the increased S100β were reactive astrocytes; the neuritic plaques were surrounded by S100β-containing astrocytes. The elevated levels of S100β provides a link between the prominent reactive gliosis and neuritic plaque formation in this common disease of the elderly and raises the possibility that S100β contributes to Alzheimer's disease neuropathology. |
doi_str_mv | 10.1016/0197-4580(92)90002-F |
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The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of aggregates of overgrown neurites in the neuritic plaques of Alzheimer's disease. The protein S100β, a neurotrophic factor produced by astroglia in the brain, induces neurite outgrowth in cerebral cortical neurons. The generation of specific S100β antibodies, the cloning of a full-length cDNA encoding the S100β mRNA, and the development of a neurite extension assay system for S100β allowed testing of the hypothesis that Alzheimer's disease S100β expression is elevated in brain temporal lobe where neuritic plaques are concentrated. The levels of S100β protein, mRNA, and specific neurotrophic activity were elevated 10–20-fold in extracts of temporal lobe from autopsy samples of Alzheimer's disease patients compared to those of aged control patients. The cells containing the increased S100β were reactive astrocytes; the neuritic plaques were surrounded by S100β-containing astrocytes. The elevated levels of S100β provides a link between the prominent reactive gliosis and neuritic plaque formation in this common disease of the elderly and raises the possibility that S100β contributes to Alzheimer's disease neuropathology.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/0197-4580(92)90002-F</identifier><identifier>PMID: 1371849</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>Aged ; Aged, 80 and over ; Aging ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Astrocytes ; Autoradiography ; Biological and medical sciences ; Cloning, Molecular ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Female ; Gliosis ; Gliosis - pathology ; Humans ; Immunoblotting ; Immunohistochemistry ; Male ; Medical sciences ; Middle Aged ; Neurites - drug effects ; Neurites - metabolism ; Neuritic plaques ; Neurology ; Neurotrophic factors ; Radioimmunoassay ; RNA - metabolism ; S100 Proteins - metabolism ; S100β ; Temporal lobe ; Temporal Lobe - metabolism ; Tissue Fixation</subject><ispartof>Neurobiology of aging, 1992, Vol.13 (1), p.1-7</ispartof><rights>1991</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-731eb9893d13f335da35a4e2127b1afc8346a0719844282532f0f59e35c65793</citedby><cites>FETCH-LOGICAL-c468t-731eb9893d13f335da35a4e2127b1afc8346a0719844282532f0f59e35c65793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0197-4580(92)90002-F$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5518383$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1371849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marshak, Daniel R.</creatorcontrib><creatorcontrib>Pesce, Susan Ann</creatorcontrib><creatorcontrib>Stanley, Laura C.</creatorcontrib><creatorcontrib>Griffin, W.Sue T.</creatorcontrib><title>Increased S100β neurotrophic activity in Alzheimer's disease temporal lobe</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>The confirming diagnosis of Alzheimer's disease includes an assessment of the concentration of neuritic plaques in the temporal lobe of the brain. The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of aggregates of overgrown neurites in the neuritic plaques of Alzheimer's disease. The protein S100β, a neurotrophic factor produced by astroglia in the brain, induces neurite outgrowth in cerebral cortical neurons. The generation of specific S100β antibodies, the cloning of a full-length cDNA encoding the S100β mRNA, and the development of a neurite extension assay system for S100β allowed testing of the hypothesis that Alzheimer's disease S100β expression is elevated in brain temporal lobe where neuritic plaques are concentrated. The levels of S100β protein, mRNA, and specific neurotrophic activity were elevated 10–20-fold in extracts of temporal lobe from autopsy samples of Alzheimer's disease patients compared to those of aged control patients. The cells containing the increased S100β were reactive astrocytes; the neuritic plaques were surrounded by S100β-containing astrocytes. The elevated levels of S100β provides a link between the prominent reactive gliosis and neuritic plaque formation in this common disease of the elderly and raises the possibility that S100β contributes to Alzheimer's disease neuropathology.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Astrocytes</subject><subject>Autoradiography</subject><subject>Biological and medical sciences</subject><subject>Cloning, Molecular</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Gliosis</subject><subject>Gliosis - pathology</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurites - drug effects</subject><subject>Neurites - metabolism</subject><subject>Neuritic plaques</subject><subject>Neurology</subject><subject>Neurotrophic factors</subject><subject>Radioimmunoassay</subject><subject>RNA - metabolism</subject><subject>S100 Proteins - metabolism</subject><subject>S100β</subject><subject>Temporal lobe</subject><subject>Temporal Lobe - metabolism</subject><subject>Tissue Fixation</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1OGzEUha2qiIbQN6DSLKoCi6G-_hnbGySECEQgsSh7y_HcEUbzk9qTSOGx-iA8EzMkojtY3cX5ztHVR8gR0DOgUPymYFQupKYnhp0aSinLZ1_IBKTUOQijvpLJO_KNHKT0NDBKqGKf7ANXoIWZkNt56yO6hGX2Byh9-Ze1uIpdH7vlY_CZ831Yh36ThTa7qJ8fMTQYj1NWhjSWsh6bZRddndXdAg_JXuXqhN93d0oeZlcPlzf53f31_PLiLvei0H2uOODCaMNL4BXnsnRcOoEMmFqAq7zmonBUgdFCMM0kZxWtpEEufSGV4VPyazu7jN3fFabeNiF5rGvXYrdKVrFxQcGnIBSMFYVgAyi2oI9dShEru4yhcXFjgdrRtR1F2lGkNcy-ubazofZjt79aNFj-L23lDvnPXe6Sd3UVXetDesekBM01H7DzLYaDs3XAaJMP2HosQ0Tf27ILH__xCv62mSU</recordid><startdate>1992</startdate><enddate>1992</enddate><creator>Marshak, Daniel R.</creator><creator>Pesce, Susan Ann</creator><creator>Stanley, Laura C.</creator><creator>Griffin, W.Sue T.</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>1992</creationdate><title>Increased S100β neurotrophic activity in Alzheimer's disease temporal lobe</title><author>Marshak, Daniel R. ; Pesce, Susan Ann ; Stanley, Laura C. ; Griffin, W.Sue T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-731eb9893d13f335da35a4e2127b1afc8346a0719844282532f0f59e35c65793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Astrocytes</topic><topic>Autoradiography</topic><topic>Biological and medical sciences</topic><topic>Cloning, Molecular</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Gliosis</topic><topic>Gliosis - pathology</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurites - drug effects</topic><topic>Neurites - metabolism</topic><topic>Neuritic plaques</topic><topic>Neurology</topic><topic>Neurotrophic factors</topic><topic>Radioimmunoassay</topic><topic>RNA - metabolism</topic><topic>S100 Proteins - metabolism</topic><topic>S100β</topic><topic>Temporal lobe</topic><topic>Temporal Lobe - metabolism</topic><topic>Tissue Fixation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marshak, Daniel R.</creatorcontrib><creatorcontrib>Pesce, Susan Ann</creatorcontrib><creatorcontrib>Stanley, Laura C.</creatorcontrib><creatorcontrib>Griffin, W.Sue T.</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marshak, Daniel R.</au><au>Pesce, Susan Ann</au><au>Stanley, Laura C.</au><au>Griffin, W.Sue T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased S100β neurotrophic activity in Alzheimer's disease temporal lobe</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>1992</date><risdate>1992</risdate><volume>13</volume><issue>1</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>The confirming diagnosis of Alzheimer's disease includes an assessment of the concentration of neuritic plaques in the temporal lobe of the brain. The presence of abnormal levels of neurotrophic factors in Alzheimer's disease is one possible explanation for the increased concentration of aggregates of overgrown neurites in the neuritic plaques of Alzheimer's disease. The protein S100β, a neurotrophic factor produced by astroglia in the brain, induces neurite outgrowth in cerebral cortical neurons. The generation of specific S100β antibodies, the cloning of a full-length cDNA encoding the S100β mRNA, and the development of a neurite extension assay system for S100β allowed testing of the hypothesis that Alzheimer's disease S100β expression is elevated in brain temporal lobe where neuritic plaques are concentrated. The levels of S100β protein, mRNA, and specific neurotrophic activity were elevated 10–20-fold in extracts of temporal lobe from autopsy samples of Alzheimer's disease patients compared to those of aged control patients. The cells containing the increased S100β were reactive astrocytes; the neuritic plaques were surrounded by S100β-containing astrocytes. The elevated levels of S100β provides a link between the prominent reactive gliosis and neuritic plaque formation in this common disease of the elderly and raises the possibility that S100β contributes to Alzheimer's disease neuropathology.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>1371849</pmid><doi>10.1016/0197-4580(92)90002-F</doi><tpages>7</tpages></addata></record> |
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subjects | Aged Aged, 80 and over Aging Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Astrocytes Autoradiography Biological and medical sciences Cloning, Molecular Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Gliosis Gliosis - pathology Humans Immunoblotting Immunohistochemistry Male Medical sciences Middle Aged Neurites - drug effects Neurites - metabolism Neuritic plaques Neurology Neurotrophic factors Radioimmunoassay RNA - metabolism S100 Proteins - metabolism S100β Temporal lobe Temporal Lobe - metabolism Tissue Fixation |
title | Increased S100β neurotrophic activity in Alzheimer's disease temporal lobe |
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