Sleep deprivation increases oleoylethanolamide in human cerebrospinal fluid

Dagmar Koethe, Daniela Schreiber, Andrea Giuffrida, Christian Mauss, Johannes Faulhaber, Bernd Heydenreich, Martin Hellmich, Rudolf Graf, Joachim Klosterkötter, Daniele Piomelli, F. Markus Leweke

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


This study investigated the role of two fatty acid ethanolamides, the endogenous cannabinoid anandamide and its structural analog oleoylethanolamide in sleep deprivation of human volunteers. Serum and cerebrospinal fluid (CSF) samples were obtained from 20 healthy volunteers before and after a night of sleep deprivation with an interval of about 12 months. We found increased levels of oleoylethanolamide in CSF (P = 0.011) but not in serum (P = 0.068) after 24 h of sleep deprivation. Oleoylethanolamide is an endogenous lipid messenger that is released after neural injury and activates peroxisome proliferator-activated receptor-α (PPAR-α) with nanomolar potency. Exogenous PPAR-α agonists, such as hypolipidemic fibrates and oleoylethanolamide, exert both neuroprotective and neurotrophic effects. Thus, our results suggest that oleoylethanolamide release may represent an endogenous neuroprotective signal during sleep deprivation.

Original languageEnglish (US)
Pages (from-to)301-305
Number of pages5
JournalJournal of Neural Transmission
Issue number3
StatePublished - Mar 2009
Externally publishedYes


  • Endocannabinoids
  • Neuroprotection
  • Oleoylethanolamide
  • Oxidative stress
  • PPAR-α
  • Sleep deprivation

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry


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