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Serum Neuron-Specific Enolase in Ischemic Brain Damage

  • M. Horn
  • W. Schlote
  • F. Seger
  • G. Oremek
Conference paper
Part of the Advances in Neurosurgery book series (NEURO, volume 21)

Abstract

Neuron-specific enolase (NSE) represents the y,y isoenzyme of the dimeric protein enolase which is a soluble enzyme of the glycolytical pathway. Physiologically, NSE is specifically present in neuronal cytoplasm and dendrites, and in cells of the amine precursor uptake and decarboxylation (APUD) cell system [5]. Since patients suffering from APUDomas, neuroblastomas, or small cell carcinoma of the lung show elevated NSE titers in serum, NSE has been clinically established as a diagnostic and prognostic marker in such neoplasms [1, 5, 8]. However, recently obtained immunohistochemical findings of a decrease in neuronal NSE immunoreactivity in experimental animals and humans following transient cerebral ischemia suggested cytoplasmic NSE loss due to ischemia [3, 6]. Previous studies have shown intracellular compounds, especially NSE, to accumulate in the extracellular fluid and cerebrospinal fluid (CSF) after ischemia [7]. The present study was performed in order to clarify if neuronal NSE release in ischemic brain damage is accompanied by an increase of NSE levels in serum. Therefore, serum NSE was measured at various times after experimental transient forebrain ischemia followed by histological evaluation of ischemic neuronal damage.

Keywords

Small Cell Carcinoma Global Cerebral Ischemia Forebrain Ischemia Ischemic Brain Damage Transient Cerebral Ischemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Cooper EH (1985) Neuron specific enolase a marker of (small cell) cancers of neuronal and neuroendocrine origin. Biomed Pharmacother 39:165–166PubMedGoogle Scholar
  2. 2.
    Hay E, Royds JA, Aelwyn G, Davies-Jone B, Lewtas NA, Timperly WR, Taylor CB (1984) Cerebrospinal fluid enolase in stroke. J Neurol Neurosurg Psychiatry 47:724–729PubMedCrossRefGoogle Scholar
  3. 3.
    Horn M, Lang C, Schlote W (1991) Delayed neuronal death caused by cardiac arrest in man. Clin Neuropathol 10:270Google Scholar
  4. 4.
    Kirino T, Sano K (1984) Selective vulnerability in the gerbil hippocampus following transient ischemia. Acta Neuropathol (Berl) 62:201–208CrossRefGoogle Scholar
  5. 5.
    Marangos PJ (1991) Neuron specific enolase as a clinical tool in neurologic and endocrine deseases. In: Gratzl M, Langley K (eds) Markers of neural and endocrine cells. VCH, Weinheim, pp 181–189Google Scholar
  6. 6.
    Matsumoto M, Yamamoto K, Homburger HA, Yanagihara T (1987) Early detection of cerebral ischemic damage and repair process in the gerbil by use of an immunohistochemical technique. Mayo Clin Proc 62:460–472PubMedGoogle Scholar
  7. 7.
    Steinberg R, Gueniau C, Scarna H, Keller A, Worcel M, Pujol JF (1984) Experimental brain ischemia: neuron-specific enolase level in cerebrospinal fluid as an index of neuronal damage. J Neurochem 43:19–24PubMedCrossRefGoogle Scholar
  8. 8.
    Wielders JPM, Bartels CT, Bank CMC, Meek JCE, van Dieijen-Visser MP, Brombacher PJ (1991) The diagnostic value of neuron-specific enolase and carcino-embryonic antigen analyses in patients with carcinoma of the lung. J Clin Chem Biochem 28:225–231Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1993

Authors and Affiliations

  • M. Horn
    • 1
  • W. Schlote
    • 2
  • F. Seger
    • 2
  • G. Oremek
    • 3
  1. 1.Neurologisches Institut (Edinger-Institut)Universität FrankfurtFrankfurt/M. 71Germany
  2. 2.Neurochirurgische KlinikUniversität WürzburgWürzburgGermany
  3. 3.Abteilung Klinische ChemieUniversität FrankfurtFrankfurt/M. 71Germany

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