Potential role of viruses in neurodegeneration
Identifieur interne : 000042 ( Ncbi/Merge ); précédent : 000041; suivant : 000043Potential role of viruses in neurodegeneration
Auteurs : Krister KristenssonSource :
- Molecular and Chemical Neuropathology [ 1044-7393 ] ; 1992.
Abstract
Viruses have the capacity to induce alterations and degenerations of neurons by different direct and indirect mechanisms. In the review, we have focused on some examples that may provide new avenues for treatment or altering the course of infections, i.e., antibodies to fusogenic virus membrane proteins, drugs that interfere with lipid metabolism, calcium channel blockers, immunoregulatory molecules, and, and inhibitors of excitotoxic amino acids. Owing to their selectivity in attack on regions of nervous tissue, governed by viral factors and by routes of invasion, viral receptors or metabolic machineries of infected cells, certain viral infections show similarities in distribution of their resulting lesions in the nervous system to that of the common human neurodegenerative diseases (namely, motor neurons disease, Parkinson’s disease, and Alzheimer’s disease). However, it should be emphasized that no infectious agent has as yet provided a complete animal model for any of these diseases, nor has any infectious agent been linked to them from observations on clinical or postomortem materials.
Url:
DOI: 10.1007/BF03159960
PubMed: 1520406
PubMed Central: 7090832
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Potential role of viruses in neurodegeneration</title><author><name sortKey="Kristensson, Krister" sort="Kristensson, Krister" uniqKey="Kristensson K" first="Krister" last="Kristensson">Krister Kristensson</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">1520406</idno><idno type="pmc">7090832</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7090832</idno><idno type="RBID">PMC:7090832</idno><idno type="doi">10.1007/BF03159960</idno><date when="1992">1992</date><idno type="wicri:Area/Pmc/Corpus">000304</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000304</idno><idno type="wicri:Area/Pmc/Curation">000304</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000304</idno><idno type="wicri:Area/Pmc/Checkpoint">000A60</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000A60</idno><idno type="wicri:Area/Ncbi/Merge">000042</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Potential role of viruses in neurodegeneration</title><author><name sortKey="Kristensson, Krister" sort="Kristensson, Krister" uniqKey="Kristensson K" first="Krister" last="Kristensson">Krister Kristensson</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Molecular and Chemical Neuropathology</title><idno type="ISSN">1044-7393</idno><imprint><date when="1992">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Viruses have the capacity to induce alterations and degenerations of neurons by different direct and indirect mechanisms. In the review, we have focused on some examples that may provide new avenues for treatment or altering the course of infections, i.e., antibodies to fusogenic virus membrane proteins, drugs that interfere with lipid metabolism, calcium channel blockers, immunoregulatory molecules, and, and inhibitors of excitotoxic amino acids. Owing to their selectivity in attack on regions of nervous tissue, governed by viral factors and by routes of invasion, viral receptors or metabolic machineries of infected cells, certain viral infections show similarities in distribution of their resulting lesions in the nervous system to that of the common human neurodegenerative diseases (namely, motor neurons disease, Parkinson’s disease, and Alzheimer’s disease). However, it should be emphasized that no infectious agent has as yet provided a complete animal model for any of these diseases, nor has any infectious agent been linked to them from observations on clinical or postomortem materials.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Allison, J" uniqKey="Allison J">J. Allison</name></author><author><name sortKey="Campbell, I L" uniqKey="Campbell I">I. L. Campbell</name></author><author><name sortKey="Morahan, G" uniqKey="Morahan G">G. Morahan</name></author><author><name sortKey="Mandel, T E" uniqKey="Mandel T">T. E. Mandel</name></author><author><name sortKey="Harrison, C" uniqKey="Harrison C">C. Harrison</name></author><author><name sortKey="Miller, J F A P" uniqKey="Miller J">J. F. A. P. Miller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Andersson, T" uniqKey="Andersson T">T. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Chem Neuropathol</journal-id><journal-id journal-id-type="iso-abbrev">Mol. Chem. Neuropathol</journal-id><journal-title-group><journal-title>Molecular and Chemical Neuropathology</journal-title></journal-title-group><issn pub-type="ppub">1044-7393</issn><publisher><publisher-name>Humana Press</publisher-name><publisher-loc>Totowa</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">1520406</article-id><article-id pub-id-type="pmc">7090832</article-id><article-id pub-id-type="publisher-id">BF03159960</article-id><article-id pub-id-type="doi">10.1007/BF03159960</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Potential role of viruses in neurodegeneration</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Kristensson</surname><given-names>Krister</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.24381.3c</institution-id><institution-id institution-id-type="ISNI">0000000092415705</institution-id><institution>Division of Basic Research in Dementia, Clinical Research Center,</institution><institution>Karolinska Institute at Huddinge Hospital,</institution></institution-wrap>Huddinge, Sweden</aff></contrib-group><pub-date pub-type="ppub"><year>1992</year></pub-date><volume>16</volume><issue>1</issue><fpage>45</fpage><lpage>58</lpage><history><date date-type="received"><day>3</day><month>5</month><year>1991</year></date><date date-type="accepted"><day>9</day><month>8</month><year>1991</year></date></history><permissions><copyright-statement>© Humana Press 1992</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1"><p>Viruses have the capacity to induce alterations and degenerations of neurons by different direct and indirect mechanisms. In the review, we have focused on some examples that may provide new avenues for treatment or altering the course of infections, i.e., antibodies to fusogenic virus membrane proteins, drugs that interfere with lipid metabolism, calcium channel blockers, immunoregulatory molecules, and, and inhibitors of excitotoxic amino acids. Owing to their selectivity in attack on regions of nervous tissue, governed by viral factors and by routes of invasion, viral receptors or metabolic machineries of infected cells, certain viral infections show similarities in distribution of their resulting lesions in the nervous system to that of the common human neurodegenerative diseases (namely, motor neurons disease, Parkinson’s disease, and Alzheimer’s disease). However, it should be emphasized that no infectious agent has as yet provided a complete animal model for any of these diseases, nor has any infectious agent been linked to them from observations on clinical or postomortem materials.</p></abstract><kwd-group xml:lang="en"><title>Index Entries</title><kwd>Virus</kwd><kwd>nervous system</kwd><kwd>neurodegenerative diseases</kwd><kwd>ALS</kwd><kwd>Alzheimer’s disease</kwd><kwd>Parkinson’s disease</kwd><kwd>Creutzfeldt-Jakob’s disease</kwd><kwd>Gerstmann-Sträussler-Scheinker syndrome</kwd><kwd>motor neuron disease</kwd><kwd>virus</kwd><kwd>prion</kwd><kwd>protein synthesis</kwd><kwd>membranes</kwd><kwd>cytoskeleton</kwd><kwd>immunologic tolerance</kwd><kwd>glutamate</kwd><kwd>lipids</kwd><kwd>calcium</kwd><kwd>excitotoxic amino acids</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© Humana Press 1992</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Kristensson, Krister" sort="Kristensson, Krister" uniqKey="Kristensson K" first="Krister" last="Kristensson">Krister Kristensson</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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