Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement
The Golgi apparatus (GA) of the anterior horn cells in the spinal cord was examined by immunohistological methods with an antibody against the MG-160 protein, a conserved intrinsic membrane sialoglycoprotein of the medial cisternae of the GA, in three patients with familial amyotrophic lateral scler...
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| Veröffentlicht in: | Journal of the neurological sciences 2000-03, Vol.174 (2), p.137-140 |
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| creator | Fujita, Yukio Okamoto, Koichi Sakurai, Atsushi Gonatas, Nicholas K Hirano, Asao |
| description | The Golgi apparatus (GA) of the anterior horn cells in the spinal cord was examined by immunohistological methods with an antibody against the MG-160 protein, a conserved intrinsic membrane sialoglycoprotein of the medial cisternae of the GA, in three patients with familial amyotrophic lateral sclerosis (FALS) with posterior column involvement. Large motor neurons in the anterior horns were markedly reduced in number and 10 of total 14 remaining large motor neurons showed fragmentation and a reduction in the number of the elements of the GA. The fragmentation of the GA was identical to that previously reported in motor neurons of the spinal cord and motor cortex from patients with sporadic ALS and in transgenic mice expressing the G93A mutation of the gene encoding the Cu/Zn superoxide dismutase months before the onset of paralysis. This is the first report of fragmented GA of the anterior horn cells in patients with FALS with posterior column involvement. The findings suggest that the GA is a common target in the neuronal degeneration in sporadic and FALS. |
| doi_str_mv | 10.1016/S0022-510X(00)00265-3 |
| format | Article |
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Large motor neurons in the anterior horns were markedly reduced in number and 10 of total 14 remaining large motor neurons showed fragmentation and a reduction in the number of the elements of the GA. The fragmentation of the GA was identical to that previously reported in motor neurons of the spinal cord and motor cortex from patients with sporadic ALS and in transgenic mice expressing the G93A mutation of the gene encoding the Cu/Zn superoxide dismutase months before the onset of paralysis. This is the first report of fragmented GA of the anterior horn cells in patients with FALS with posterior column involvement. The findings suggest that the GA is a common target in the neuronal degeneration in sporadic and FALS.</description><identifier>ISSN: 0022-510X</identifier><identifier>EISSN: 1878-5883</identifier><identifier>DOI: 10.1016/S0022-510X(00)00265-3</identifier><identifier>PMID: 10727699</identifier><identifier>CODEN: JNSCAG</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Amino Acid Substitution ; Anterior Horn Cells - pathology ; Biological and medical sciences ; Biomarkers ; Codon - genetics ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Familial amyotrophic lateral sclerosis ; Golgi apparatus ; Golgi Apparatus - ultrastructure ; Humans ; Medical sciences ; MG-160 ; Motor Neuron Disease - enzymology ; Motor Neuron Disease - genetics ; Motor Neuron Disease - pathology ; Nerve Degeneration ; Nerve Tissue Proteins - analysis ; Neurology ; Pathology ; Point Mutation ; Receptors, Cell Surface ; Receptors, Fibroblast Growth Factor ; Sialoglycoproteins - analysis ; SOD1 gene ; Spinal cord ; Spinal Cord - pathology ; Superoxide Dismutase - genetics</subject><ispartof>Journal of the neurological sciences, 2000-03, Vol.174 (2), p.137-140</ispartof><rights>2000 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-2f675de49b77acbe5976d7ae95148fc3427a22d41269648db4199ee66aeabd833</citedby><cites>FETCH-LOGICAL-c442t-2f675de49b77acbe5976d7ae95148fc3427a22d41269648db4199ee66aeabd833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0022-510X(00)00265-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1335358$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10727699$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fujita, Yukio</creatorcontrib><creatorcontrib>Okamoto, Koichi</creatorcontrib><creatorcontrib>Sakurai, Atsushi</creatorcontrib><creatorcontrib>Gonatas, Nicholas K</creatorcontrib><creatorcontrib>Hirano, Asao</creatorcontrib><title>Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement</title><title>Journal of the neurological sciences</title><addtitle>J Neurol Sci</addtitle><description>The Golgi apparatus (GA) of the anterior horn cells in the spinal cord was examined by immunohistological methods with an antibody against the MG-160 protein, a conserved intrinsic membrane sialoglycoprotein of the medial cisternae of the GA, in three patients with familial amyotrophic lateral sclerosis (FALS) with posterior column involvement. Large motor neurons in the anterior horns were markedly reduced in number and 10 of total 14 remaining large motor neurons showed fragmentation and a reduction in the number of the elements of the GA. The fragmentation of the GA was identical to that previously reported in motor neurons of the spinal cord and motor cortex from patients with sporadic ALS and in transgenic mice expressing the G93A mutation of the gene encoding the Cu/Zn superoxide dismutase months before the onset of paralysis. This is the first report of fragmented GA of the anterior horn cells in patients with FALS with posterior column involvement. The findings suggest that the GA is a common target in the neuronal degeneration in sporadic and FALS.</description><subject>Amino Acid Substitution</subject><subject>Anterior Horn Cells - pathology</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Codon - genetics</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Familial amyotrophic lateral sclerosis</subject><subject>Golgi apparatus</subject><subject>Golgi Apparatus - ultrastructure</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>MG-160</subject><subject>Motor Neuron Disease - enzymology</subject><subject>Motor Neuron Disease - genetics</subject><subject>Motor Neuron Disease - pathology</subject><subject>Nerve Degeneration</subject><subject>Nerve Tissue Proteins - analysis</subject><subject>Neurology</subject><subject>Pathology</subject><subject>Point Mutation</subject><subject>Receptors, Cell Surface</subject><subject>Receptors, Fibroblast Growth Factor</subject><subject>Sialoglycoproteins - analysis</subject><subject>SOD1 gene</subject><subject>Spinal cord</subject><subject>Spinal Cord - pathology</subject><subject>Superoxide Dismutase - genetics</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1TAQhiMEoofCI4C8QAgWATsXX1YIFVqQKnVRkNhZc5xJj5ETB9s5qO_EQ-I04bJjZXn0_fPPzF8UTxl9zSjjb64praqyZfTrS0pf5Q9vy_pesWNSyLKVsr5f7P4gJ8WjGL9RSrmU6mFxwqioBFdqV_w8D3Az4JggWT8S35N0QHLh3Y0lME0QIM3xdxnGhMH6QA4-jMSgc5HYkUxZmztE8sOmA-lhsM6CIzDc-hT8dLCGOMjKXIvGYfDRbuz11XtGhnk1j7l_RyYfNxPj3TyM2eDo3RGXGR8XD3pwEZ9s72nx5fzD57OP5eXVxaezd5elaZoqlVXPRdtho_ZCgNljqwTvBKBqWSN7UzeVgKrqGlZxxRvZ7RumFCLngLDvZF2fFi_WvlPw32eMSQ82LuvCiH6OWlAlZNWoDLYraPJSMWCvp2AHCLeaUb3EpO9i0ksGmlJ9F5NeDJ5tBvN-wO4f1ZpLBp5vAEQDrg8wGhv_cnXd1q3M2NsVw3yNo8Wgo8lRGOxsQJN05-1_JvkFwGWzyw</recordid><startdate>20000315</startdate><enddate>20000315</enddate><creator>Fujita, Yukio</creator><creator>Okamoto, Koichi</creator><creator>Sakurai, Atsushi</creator><creator>Gonatas, Nicholas K</creator><creator>Hirano, Asao</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20000315</creationdate><title>Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement</title><author>Fujita, Yukio ; Okamoto, Koichi ; Sakurai, Atsushi ; Gonatas, Nicholas K ; Hirano, Asao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-2f675de49b77acbe5976d7ae95148fc3427a22d41269648db4199ee66aeabd833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Amino Acid Substitution</topic><topic>Anterior Horn Cells - pathology</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Codon - genetics</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Familial amyotrophic lateral sclerosis</topic><topic>Golgi apparatus</topic><topic>Golgi Apparatus - ultrastructure</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>MG-160</topic><topic>Motor Neuron Disease - enzymology</topic><topic>Motor Neuron Disease - genetics</topic><topic>Motor Neuron Disease - pathology</topic><topic>Nerve Degeneration</topic><topic>Nerve Tissue Proteins - analysis</topic><topic>Neurology</topic><topic>Pathology</topic><topic>Point Mutation</topic><topic>Receptors, Cell Surface</topic><topic>Receptors, Fibroblast Growth Factor</topic><topic>Sialoglycoproteins - analysis</topic><topic>SOD1 gene</topic><topic>Spinal cord</topic><topic>Spinal Cord - pathology</topic><topic>Superoxide Dismutase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fujita, Yukio</creatorcontrib><creatorcontrib>Okamoto, Koichi</creatorcontrib><creatorcontrib>Sakurai, Atsushi</creatorcontrib><creatorcontrib>Gonatas, Nicholas K</creatorcontrib><creatorcontrib>Hirano, Asao</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>MEDLINE - Academic</collection><jtitle>Journal of the neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fujita, Yukio</au><au>Okamoto, Koichi</au><au>Sakurai, Atsushi</au><au>Gonatas, Nicholas K</au><au>Hirano, Asao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement</atitle><jtitle>Journal of the neurological sciences</jtitle><addtitle>J Neurol Sci</addtitle><date>2000-03-15</date><risdate>2000</risdate><volume>174</volume><issue>2</issue><spage>137</spage><epage>140</epage><pages>137-140</pages><issn>0022-510X</issn><eissn>1878-5883</eissn><coden>JNSCAG</coden><abstract>The Golgi apparatus (GA) of the anterior horn cells in the spinal cord was examined by immunohistological methods with an antibody against the MG-160 protein, a conserved intrinsic membrane sialoglycoprotein of the medial cisternae of the GA, in three patients with familial amyotrophic lateral sclerosis (FALS) with posterior column involvement. Large motor neurons in the anterior horns were markedly reduced in number and 10 of total 14 remaining large motor neurons showed fragmentation and a reduction in the number of the elements of the GA. The fragmentation of the GA was identical to that previously reported in motor neurons of the spinal cord and motor cortex from patients with sporadic ALS and in transgenic mice expressing the G93A mutation of the gene encoding the Cu/Zn superoxide dismutase months before the onset of paralysis. This is the first report of fragmented GA of the anterior horn cells in patients with FALS with posterior column involvement. The findings suggest that the GA is a common target in the neuronal degeneration in sporadic and FALS.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>10727699</pmid><doi>10.1016/S0022-510X(00)00265-3</doi><tpages>4</tpages></addata></record> |
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| subjects | Amino Acid Substitution Anterior Horn Cells - pathology Biological and medical sciences Biomarkers Codon - genetics Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Familial amyotrophic lateral sclerosis Golgi apparatus Golgi Apparatus - ultrastructure Humans Medical sciences MG-160 Motor Neuron Disease - enzymology Motor Neuron Disease - genetics Motor Neuron Disease - pathology Nerve Degeneration Nerve Tissue Proteins - analysis Neurology Pathology Point Mutation Receptors, Cell Surface Receptors, Fibroblast Growth Factor Sialoglycoproteins - analysis SOD1 gene Spinal cord Spinal Cord - pathology Superoxide Dismutase - genetics |
| title | Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement |
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