ABSTRACT
After the discovery of a hypocretin-2 receptor gene mutation in canine narcolepsy and the observation of a narcolepsy-like phenotype in prepro-hypocretin gene knock-out mice, a disturbed hypocretin transmission was searched also in human narcolepsy. Using a radioimmuno assay (RIA) the Stanford group in January 2000 first described the absence of the peptide hypocretin-1 in the cerebrospinal fluid (CSF) of seven out of nine patients with narcolepsy from Leiden (Holland) (1). This result was confirmed in a larger group of patients from Stanford, Hattiesburg, Atlanta (US), Leiden, Zurich (Switzerland), Prague (Czech Republic) and Trondheim (Norway), again tested in Stanford (2), as well as in a third group of patients from Zu¨rich and Montpellier (France), this time tested in Zurich (3). Measurements of CSF hypocretin-2 levels in human narcolepsy were reported only once in the literature but remained, so far, unconfirmed (4).
