CSF beta-amyloid levels are altered in narcolepsy: A link with the inflammatory hypothesis?

Claudio Liguori, Fabio Placidi, Maria Albanese, Marzia Nuccetelli, Francesca Izzi, Maria Grazia Marciani, Nicola Biagio Mercuri, Sergio Bernardini, Andrea Romigi

Research output: Contribution to journalArticlepeer-review


Narcolepsy is characterized by hypocretin deficiency due to the loss of hypothalamic orexinergic neurons, and is associated with both the human leucocyte antigen DQB1*06:02 and the T cell receptor polymorphism. The above relationship suggests autoimmune/inflammatory processes underlying the loss of orexinergic neurons in narcolepsy. To test the autoimmune/inflammatory hypothesis by means of cerebrospinal fluid (CSF) levels of beta-amyloid1-42 and/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta-amyloid1-42 CSF levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of CSF beta-amyloid1-42 (-1) in six of 16 narcoleptic patients (37.5%). We hypothesize that the significant decrease of the CSF beta-amyloid1-42 levels in narcoleptic patients may support both the inflammatory/autoimmune hypothesis as the basis of the pathogenesis of narcolepsy and the prevalence of an 'amyloidogenic' pathway caused by the deficiency of the alpha-secretases enzymes.

Original languageEnglish
Pages (from-to)420-424
Number of pages5
JournalJournal of Sleep Research
Issue number4
Publication statusPublished - 2014


  • CSF
  • Narcolepsy
  • Orexin

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Cognitive Neuroscience
  • Medicine(all)


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