Inflammatory processes in amyotrophic lateral sclerosis
Neuroinflammation is a characteristic of pathologically affected tissue in several neurodegenerative disorders. These changes can be observed in the brainstem and spinal cord of amyotrophic lateral sclerosis (ALS) cases and in mouse models of the disease. They include an accumulation of large number...
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Veröffentlicht in: | Muscle & nerve 2002-10, Vol.26 (4), p.459-470 |
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description | Neuroinflammation is a characteristic of pathologically affected tissue in several neurodegenerative disorders. These changes can be observed in the brainstem and spinal cord of amyotrophic lateral sclerosis (ALS) cases and in mouse models of the disease. They include an accumulation of large numbers of activated microglia and astrocytes, as well as small numbers of T cells, mostly adhering to postcapillary venules. Accompanying biochemical alterations include the appearance of numerous molecules characteristic of free‐radical attack, the occurrence of proteins associated with activation of the complement cascade, and a sharp upregulation of the enzyme cyclooxygenase 2 (COX‐2). Anti‐inflammatory agents may have a role to play in treating ALS. COX‐2 is a particularly attractive target because of its marked increase in ALS spinal cord. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 459–470, 2002 |
doi_str_mv | 10.1002/mus.10191 |
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Muscle Nerve 26: 459–470, 2002</description><identifier>ISSN: 0148-639X</identifier><identifier>EISSN: 1097-4598</identifier><identifier>DOI: 10.1002/mus.10191</identifier><identifier>PMID: 12362410</identifier><identifier>CODEN: MUNEDE</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Amyotrophic Lateral Sclerosis - etiology ; Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - pathology ; Amyotrophic Lateral Sclerosis - therapy ; Animals ; astrocytes ; Biological and medical sciences ; complement ; cyclooxygenase ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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L.</creatorcontrib><creatorcontrib>McGeer, E. G.</creatorcontrib><title>Inflammatory processes in amyotrophic lateral sclerosis</title><title>Muscle & nerve</title><addtitle>Muscle Nerve</addtitle><description>Neuroinflammation is a characteristic of pathologically affected tissue in several neurodegenerative disorders. These changes can be observed in the brainstem and spinal cord of amyotrophic lateral sclerosis (ALS) cases and in mouse models of the disease. They include an accumulation of large numbers of activated microglia and astrocytes, as well as small numbers of T cells, mostly adhering to postcapillary venules. Accompanying biochemical alterations include the appearance of numerous molecules characteristic of free‐radical attack, the occurrence of proteins associated with activation of the complement cascade, and a sharp upregulation of the enzyme cyclooxygenase 2 (COX‐2). Anti‐inflammatory agents may have a role to play in treating ALS. COX‐2 is a particularly attractive target because of its marked increase in ALS spinal cord. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 459–470, 2002</description><subject>Amyotrophic Lateral Sclerosis - etiology</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - pathology</subject><subject>Amyotrophic Lateral Sclerosis - therapy</subject><subject>Animals</subject><subject>astrocytes</subject><subject>Biological and medical sciences</subject><subject>complement</subject><subject>cyclooxygenase</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Humans</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Medical sciences</subject><subject>microglia</subject><subject>Neurology</subject><subject>superoxide dismutase</subject><issn>0148-639X</issn><issn>1097-4598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtOwzAQBVALgWh5LPgBlA1ILEI9fsTxEiFeEpRKFMHOclxHBJymeFJB_56UFlixshdnZq4uIQdAT4FSNqjn2H1AwwbpA9UqFVLnm6RPQeRpxvVzj-wgvlJKIc_UNukB4xkTQPtE3UzLYOvatk1cJLPYOI_oMammia0XTRub2UvlkmBbH21I0AUfG6xwj2yVNqDfX7-75PHyYnx-nd7eX92cn92mTkgJKUw85TlIwVRhlS3txDlXFoWiwtOCyxxKPVFdKKVY4ZhW0jEptIAcsowKxnfJ8WpvF-197rE1dYXOh2CnvpmjUQwkCK06eLKCrsuH0ZdmFqvaxoUBapYtma4l891SZw_XS-dF7Sd_cl1LB47WwKKzoYx26ir8c1zLLOdLN1i5jyr4xf8Xzd3jw8_pdDVRYes_fydsfDOZ4kqap-GV0dmQjdhobBT_AsBbjHg</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>McGeer, P. L.</creator><creator>McGeer, E. G.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><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>200210</creationdate><title>Inflammatory processes in amyotrophic lateral sclerosis</title><author>McGeer, P. L. ; McGeer, E. G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4551-1de03815427ba7afadcccfbb704e0b3581f9d7867772bc2975c25494181660423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Amyotrophic Lateral Sclerosis - etiology</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - pathology</topic><topic>Amyotrophic Lateral Sclerosis - therapy</topic><topic>Animals</topic><topic>astrocytes</topic><topic>Biological and medical sciences</topic><topic>complement</topic><topic>cyclooxygenase</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Humans</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Medical sciences</topic><topic>microglia</topic><topic>Neurology</topic><topic>superoxide dismutase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGeer, P. L.</creatorcontrib><creatorcontrib>McGeer, E. G.</creatorcontrib><collection>Istex</collection><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>Muscle & nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McGeer, P. L.</au><au>McGeer, E. G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammatory processes in amyotrophic lateral sclerosis</atitle><jtitle>Muscle & nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>2002-10</date><risdate>2002</risdate><volume>26</volume><issue>4</issue><spage>459</spage><epage>470</epage><pages>459-470</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>Neuroinflammation is a characteristic of pathologically affected tissue in several neurodegenerative disorders. These changes can be observed in the brainstem and spinal cord of amyotrophic lateral sclerosis (ALS) cases and in mouse models of the disease. They include an accumulation of large numbers of activated microglia and astrocytes, as well as small numbers of T cells, mostly adhering to postcapillary venules. Accompanying biochemical alterations include the appearance of numerous molecules characteristic of free‐radical attack, the occurrence of proteins associated with activation of the complement cascade, and a sharp upregulation of the enzyme cyclooxygenase 2 (COX‐2). Anti‐inflammatory agents may have a role to play in treating ALS. COX‐2 is a particularly attractive target because of its marked increase in ALS spinal cord. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 459–470, 2002</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12362410</pmid><doi>10.1002/mus.10191</doi><tpages>12</tpages></addata></record> |
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subjects | Amyotrophic Lateral Sclerosis - etiology Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - pathology Amyotrophic Lateral Sclerosis - therapy Animals astrocytes Biological and medical sciences complement cyclooxygenase Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Humans Inflammation - metabolism Inflammation - pathology Medical sciences microglia Neurology superoxide dismutase |
title | Inflammatory processes in amyotrophic lateral sclerosis |
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