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Volume 17 Supplement 4

Sepsis 2013

  • Poster presentation
  • Open Access

Brain markers of neurodegeneration in sepsis survivor rats

  • 1,
  • 1,
  • 2,
  • 3,
  • 2,
  • 1,
  • 1,
  • 3,
  • 1,
  • 2,
  • 2 and
  • 1
Critical Care201317 (Suppl 4) :P87

https://doi.org/10.1186/cc12986

  • Published:

Keywords

  • Nitric Oxide
  • Prefrontal Cortex
  • Inhibitory Avoidance
  • Hippocampal Atrophy
  • Cecal Ligation

Background

Several preclinical and clinical reports indicate a significant role for systemic inflammation in chronic neurodegenerative diseases [1], with commitment of different brain regions. Several studies have demonstrated hippocampal atrophy, EEG changes [2], profound glial activation, the generation of nitric oxide and changes in expression of mediator apoptosis [3]. The release of these mediators and oxidative stress occur mainly in acute phase inflammation in sepsis survivor rats and are associated with long-term cognitive impairment [4]. These cognitive deficits have been associated with decreased quality of life and increased long-term morbidity. Some of these alterations resembled the pathophysiological mechanisms of neurodegenerative diseases. For this reason, we analyzed parameters related to neurodegeneration in rats that survived sepsis, and their relation to cognitive dysfunction.

Materials and methods

Wistar rats were subjected to sepsis by cecal ligation and puncture and 30 days after surgery the hippocampus and prefrontal cortex were isolated just after cognitive evaluation by the inhibitory avoidance test. The immunocontent of β-amyloid peptide (Aβ), receptor for advanced glycation endproducts (RAGE) and synaptophysin were analyzed by western blot.

Results

Aβ was increased in septic animals in the hippocampus, but not in the prefrontal cortex. RAGE was upregulated in both structures after sepsis, and the immunocontent of synaptophysin was decreased only in the prefrontal, and inversely correlated to Aβ levels. Prefrontal levels of synaptophysin correlated with performance in the inhibitory avoidance.

Conclusions

The brain from sepsis survivor animals presented several markers of neurodegeneration, and inhibitory avoidance test performance seems to be dependent on the levels at some of these markers.

Declarations

Acknowledgements

Supported by grants from the National Council for Scientific and Technological Development (CNPq), FAPERGS PqG 2010 (1008860) and Universidade do Extremo Sul Catarinense.

Authors’ Affiliations

(1)
University of the Extreme-South Catarinense, Criciúma, Brazil
(2)
Federal University of the Rio Grande do Sul (UFRGS), Porto Alegre, Brazil
(3)
University of Southern Santa Catarina, Tubarão, Brazil

References

  1. Cunningham C: Microglia and neurodegeneration: the role of systemic inflammation. Glia 2013, 61: 71-90. 10.1002/glia.22350View ArticlePubMedGoogle Scholar
  2. Semmler A, Widmann CN, Okulla T, Urbach H, Kaiser M, Widman G, Mormann F, Weide J, Fliessbach K, Hoeft A, Jessen F, Putensen C, Heneka MT: Persistent cognitive impairment, hippocampal atrophy and EEG changes in sepsis survivors. J Neurol Neurosurg Psychiatry 2013, 84: 62-69. 10.1136/jnnp-2012-302883View ArticlePubMedGoogle Scholar
  3. Semmler A, Okulla T, Sastre M, Dumitrescu-Ozimek L, Heneka MT: Systemic inflammation induces apoptosis with variable vulnerability of different brain regions. J Chem Neuroanat 2005, 30: 144-157. 10.1016/j.jchemneu.2005.07.003View ArticlePubMedGoogle Scholar
  4. Biff D, Petronilho F, Constantino L, Vuolo F, Zamora-Berridi GJ, Dall'igna DM, Comim CM, Quevedo J, Kaczinski F, Dal-Pizzol F: Correlation of acute phase inflammatory and oxidative markers with long-term cognitive impairment in sepsis survivors rats. Shock 2013, 40: 45-48. 10.1097/SHK.0b013e3182959cfaView ArticlePubMedGoogle Scholar

Copyright

© de Souza Constantino et al.; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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