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Potential role of viruses in neurodegeneration

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 prot...

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Detalles Bibliográficos
Autor principal: Kristensson, Krister
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Humana Press 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7090832/
https://www.ncbi.nlm.nih.gov/pubmed/1520406
http://dx.doi.org/10.1007/BF03159960
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author Kristensson, Krister
author_facet Kristensson, Krister
author_sort Kristensson, Krister
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description 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.
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spelling pubmed-70908322020-03-24 Potential role of viruses in neurodegeneration Kristensson, Krister Mol Chem Neuropathol Original Articles 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. Humana Press 1992 /pmc/articles/PMC7090832/ /pubmed/1520406 http://dx.doi.org/10.1007/BF03159960 Text en © Humana Press 1992 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.
spellingShingle Original Articles
Kristensson, Krister
Potential role of viruses in neurodegeneration
title Potential role of viruses in neurodegeneration
title_full Potential role of viruses in neurodegeneration
title_fullStr Potential role of viruses in neurodegeneration
title_full_unstemmed Potential role of viruses in neurodegeneration
title_short Potential role of viruses in neurodegeneration
title_sort potential role of viruses in neurodegeneration
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7090832/
https://www.ncbi.nlm.nih.gov/pubmed/1520406
http://dx.doi.org/10.1007/BF03159960
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