Literature DB >> 9003413

Marked increases in concentrations of apolipoprotein in the cerebrospinal fluid of poliovirus-infected macaques: relations between apolipoprotein concentrations and severity of brain injury.

K Saito1, M Seishima, M P Heyes, H Song, S Fujigaki, S Maeda, J H Vickers, A Noma.   

Abstract

Apolipoproteins in cerebrospinal fluid (CSF) might have important functional roles in the pathophysiology of brain and lipid metabolism in the vascular component. The present study examined apolipoprotein A-I (apo-A-I) and apolipoprotein E (apo-E) levels in CSF and serum from poliovirus-infected macaques. Poliovirus-infected macaques developed motor deficits and were classified into three groups: (1) muscle weakness in one or both legs; (2) partial paralysis in one or both legs; (3) complete paralysis in one or both legs. No motor deficits were evident in the control or sham-treated macaques. Apo-A-I concentrations in CSF were markedly elevated in poliovirus-infected macaques with weakness, partial or complete paralysis, in comparison with either control or sham-treated animals, and were proportional to the severity of motor impairment. Apo-E concentrations in CSF were also significantly elevated in poliovirus-infected macaques with complete paralysis. The magnitude of increase in CSF apo-A-I or apo-E concentrations was also closely associated with the degree of histologic neurological damage and inflammation (lesion scores). However, no changes in serum apo-A-I and apo-E concentrations were observed in the poliovirus-infected macaques compared with control macaques. Furthermore there were no significant correlations apo-A-I or apo-E concentrations between serum and CSF. We hypothesize that the elevation of apo-A-I and apo-E concentrations after poliovirus infection is caused by immune stimulation within the central nervous system (CNS). Measures of CSF apo-A-I and apo-E levels might serve as a useful marker for the severity and/or the range of CNS injury.

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Year:  1997        PMID: 9003413      PMCID: PMC1218048          DOI: 10.1042/bj3210145

Source DB:  PubMed          Journal:  Biochem J        ISSN: 0264-6021            Impact factor:   3.857


  17 in total

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  6 in total

Review 1.  Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration.

Authors:  Jeriel T R Keeney; Aaron M Swomley; Sarah Förster; Jessica L Harris; Rukhsana Sultana; D Allan Butterfield
Journal:  Proteomics Clin Appl       Date:  2013-01       Impact factor: 3.494

2.  An ABCA1-independent pathway for recycling a poorly lipidated 8.1 nm apolipoprotein E particle from glia.

Authors:  Jianjia Fan; Sophie Stukas; Charmaine Wong; Jennifer Chan; Sharon May; Nicole DeValle; Veronica Hirsch-Reinshagen; Anna Wilkinson; Michael N Oda; Cheryl L Wellington
Journal:  J Lipid Res       Date:  2011-06-26       Impact factor: 5.922

Review 3.  HDL and cognition in neurodegenerative disorders.

Authors:  David A Hottman; Dustin Chernick; Shaowu Cheng; Zhe Wang; Ling Li
Journal:  Neurobiol Dis       Date:  2014-08-13       Impact factor: 5.996

4.  Levels of apolipoprotein A-II in cerebrospinal fluid in patients with neuroborreliosis are associated with lipophagocytosis.

Authors:  L Táborský; P Adam; O Sobek; M Dostál; J Dvoráková; L Dubská
Journal:  Folia Microbiol (Praha)       Date:  2003       Impact factor: 2.099

5.  Intravenously injected human apolipoprotein A-I rapidly enters the central nervous system via the choroid plexus.

Authors:  Sophie Stukas; Jerome Robert; Michael Lee; Iva Kulic; Michael Carr; Katherine Tourigny; Jianjia Fan; Dhananjay Namjoshi; Kalistyne Lemke; Nicole DeValle; Jeniffer Chan; Tammy Wilson; Anna Wilkinson; Rafi Chapanian; Jayachandran N Kizhakkedathu; John R Cirrito; Michael N Oda; Cheryl L Wellington
Journal:  J Am Heart Assoc       Date:  2014-11-12       Impact factor: 5.501

6.  Apolipoprotein A1 in Cerebrospinal Fluid Is Insufficient to Distinguish Alzheimer's Disease from Other Dementias in a Naturalistic, Clinical Setting.

Authors:  Nicolai Maximilian Stoye; Patrick Jung; Malena Dos Santos Guilherme; Johannes Lotz; Andreas Fellgiebel; Kristina Endres
Journal:  J Alzheimers Dis Rep       Date:  2020-02-04
  6 in total

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