FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2147089471> ?p ?o ?g. }

• W2147089471 endingPage "173" @default.
• W2147089471 startingPage "162" @default.
• W2147089471 abstract "Axonal damage is a correlate for increasing disability in multiple sclerosis. Animal models such as experimental autoimmune encephalomyelitis (EAE) may help to develop better therapeutical neuroprotective strategies for the human disease. Here we investigate the pattern of axonal injury in murine myelin oligodendrocyte glycoprotein peptide 35–55 (MOG) induced EAE. Inflammatory infiltration, axonal densities and expression of amyloid precursor protein (APP), neurofilaments (SMI31 and 32) as well as expression of sodium channels were quantified in lesions, the perilesional area and normal appearing white matter (NAWM). Quantification of T cells and macrophages revealed a significant reduction of inflammatory infiltration at later disease stages despite an increase of demyelinated areas and persistent clinical disability. In lesions, axonal density was already significantly reduced early and throughout all investigated disease stages. A significant axonal loss was also seen in the grey matter and at later time points in the perilesion as well as NAWM. Numbers of axons characterized by non-phosphorylated neurofilaments and re-distribution of sodium channels 1.2 and 1.6 increased over the course of MOG-EAE whilst APP positive axons peaked at the maximum of disease. Finally, double-labeling experiments revealed a strong colocalization of sodium channels with APP, neurofilaments and the axonal nodal protein Caspr, but not glial and myelin markers in actively demyelinating lesions. In summary, progressive axonal loss distant from lesions is mainly associated with changes in neurofilament phosphorylation, re-distribution of sodium channels and demyelination. This axonal loss is dissociated from acute inflammatory infiltration and markedly correlates with clinical impairment. Consequently, therapeutic intervention may be promising at early stages of EAE focusing on inflammation, or later in disease targeting degenerative mechanisms." @default.
• W2147089471 created "2016-06-24" @default.
• W2147089471 creator A5000857311 @default.
• W2147089471 creator A5005920666 @default.
• W2147089471 creator A5062220148 @default.
• W2147089471 creator A5073178395 @default.
• W2147089471 date "2008-05-01" @default.
• W2147089471 modified "2023-09-29" @default.
• W2147089471 title "Pattern of axonal injury in murine myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis: Implications for multiple sclerosis" @default.
• W2147089471 cites W1500818454 @default.
• W2147089471 cites W1879457624 @default.
• W2147089471 cites W1933220919 @default.
• W2147089471 cites W1937650001 @default.
• W2147089471 cites W1965198549 @default.
• W2147089471 cites W1966744945 @default.
• W2147089471 cites W197245174 @default.
• W2147089471 cites W1985989596 @default.
• W2147089471 cites W1986436947 @default.
• W2147089471 cites W1998009350 @default.
• W2147089471 cites W2012283308 @default.
• W2147089471 cites W2013973364 @default.
• W2147089471 cites W2025732446 @default.
• W2147089471 cites W2039380715 @default.
• W2147089471 cites W2042435361 @default.
• W2147089471 cites W2044383319 @default.
• W2147089471 cites W2058214824 @default.
• W2147089471 cites W2061039466 @default.
• W2147089471 cites W2064262911 @default.
• W2147089471 cites W2064286651 @default.
• W2147089471 cites W2074582763 @default.
• W2147089471 cites W2077610348 @default.
• W2147089471 cites W2079076181 @default.
• W2147089471 cites W2080704680 @default.
• W2147089471 cites W2082363371 @default.
• W2147089471 cites W2087249766 @default.
• W2147089471 cites W2108335498 @default.
• W2147089471 cites W2113101274 @default.
• W2147089471 cites W2118296597 @default.
• W2147089471 cites W2119260372 @default.
• W2147089471 cites W2122347714 @default.
• W2147089471 cites W2133349263 @default.
• W2147089471 cites W2137911312 @default.
• W2147089471 cites W2139082112 @default.
• W2147089471 cites W2139843103 @default.
• W2147089471 cites W2140017053 @default.
• W2147089471 cites W2143144699 @default.
• W2147089471 cites W2144235003 @default.
• W2147089471 cites W2145657433 @default.
• W2147089471 cites W2148631447 @default.
• W2147089471 cites W2155221060 @default.
• W2147089471 cites W2158424311 @default.
• W2147089471 cites W2158796001 @default.
• W2147089471 cites W2168506147 @default.
• W2147089471 cites W2312603198 @default.
• W2147089471 cites W2325038063 @default.
• W2147089471 cites W2325735106 @default.
• W2147089471 cites W2331930580 @default.
• W2147089471 cites W4252049794 @default.
• W2147089471 cites W82941739 @default.
• W2147089471 cites W87687135 @default.
• W2147089471 cites W88568342 @default.
• W2147089471 doi "https://doi.org/10.1016/j.nbd.2008.01.001" @default.
• W2147089471 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18342527" @default.
• W2147089471 hasPublicationYear "2008" @default.
• W2147089471 type Work @default.
• W2147089471 sameAs 2147089471 @default.
• W2147089471 citedByCount "111" @default.
• W2147089471 countsByYear W21470894712012 @default.
• W2147089471 countsByYear W21470894712013 @default.
• W2147089471 countsByYear W21470894712014 @default.
• W2147089471 countsByYear W21470894712015 @default.
• W2147089471 countsByYear W21470894712016 @default.
• W2147089471 countsByYear W21470894712017 @default.
• W2147089471 countsByYear W21470894712018 @default.
• W2147089471 countsByYear W21470894712019 @default.
• W2147089471 countsByYear W21470894712020 @default.
• W2147089471 countsByYear W21470894712021 @default.
• W2147089471 countsByYear W21470894712022 @default.
• W2147089471 countsByYear W21470894712023 @default.
• W2147089471 crossrefType "journal-article" @default.
• W2147089471 hasAuthorship W2147089471A5000857311 @default.
• W2147089471 hasAuthorship W2147089471A5005920666 @default.
• W2147089471 hasAuthorship W2147089471A5062220148 @default.
• W2147089471 hasAuthorship W2147089471A5073178395 @default.
• W2147089471 hasConcept C126838900 @default.
• W2147089471 hasConcept C142724271 @default.
• W2147089471 hasConcept C143409427 @default.
• W2147089471 hasConcept C157207234 @default.
• W2147089471 hasConcept C169760540 @default.
• W2147089471 hasConcept C203014093 @default.
• W2147089471 hasConcept C204232928 @default.
• W2147089471 hasConcept C2776985911 @default.
• W2147089471 hasConcept C2778486448 @default.
• W2147089471 hasConcept C2778609137 @default.
• W2147089471 hasConcept C2779357208 @default.
• W2147089471 hasConcept C2779530196 @default.
• W2147089471 hasConcept C2780640218 @default.
• W2147089471 hasConcept C2780876595 @default.

• next