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- W103760963 startingPage "367" @default.
- W103760963 abstract "Soon after the discovery of narcolepsy genes in dogs (hypocretin receptor 2 [hcrtr-2]) (1) and mice (preprohypocretin) (2), it was determined that most (about 90%) human narcolepsy is associated with hypocretin/orexin ligand deficiency (3–5). The hypocretin/orexin ligand deficiency in humans is probably owing to the acquired cell death of hypocretin-containing neurons, which is triggered for several reasons: (1) the onset of narcolepsy in humans is in the late developmental years (i.e., puberty) (6), whereas in narcoleptic animals with hypocretin-related gene mutations onset is in the much earlier, developmental years (2,7); and (2) mice/rats with postnatally ablated hypocretin-containing neurons (orexin/ataxin-3 transgenic) exhibit a narcolepsy phenotype (cataplexy, sleep fragmentation, and tendency to obesity) similar to that of human narcolepsy (8)." @default.
- W103760963 created "2016-06-24" @default.
- W103760963 creator A5057374465 @default.
- W103760963 creator A5060824249 @default.
- W103760963 date "2006-01-01" @default.
- W103760963 modified "2023-09-26" @default.
- W103760963 title "Hypocretin/Orexin Replacement Therapy in Hypocretin/Orexin-Deficient Narcolepsy" @default.
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