Peyron C, Faraco J, Rogers W, Ripley B, Overeem S, Charnay Y, Nevsimalova S, Aldrich M, Reynolds D, Albin R, Li R, Hungs M, Pedrazzoli M, Padigaru M, Kucherlapati M, Fan J, Maki R, Lammers G J, Bouras C, Kucherlapati R, Nishino S, Mignot E
Center for Narcolepsy, Stanford University Medical School 1201 Welch Road, Stanford, California 94305-5485, USA.
Nat Med. 2000 Sep;6(9):991-7. doi: 10.1038/79690.
We explored the role of hypocretins in human narcolepsy through histopathology of six narcolepsy brains and mutation screening of Hcrt, Hcrtr1 and Hcrtr2 in 74 patients of various human leukocyte antigen and family history status. One Hcrt mutation, impairing peptide trafficking and processing, was found in a single case with early onset narcolepsy. In situ hybridization of the perifornical area and peptide radioimmunoassays indicated global loss of hypocretins, without gliosis or signs of inflammation in all human cases examined. Although hypocretin loci do not contribute significantly to genetic predisposition, most cases of human narcolepsy are associated with a deficient hypocretin system.
我们通过对六个发作性睡病患者大脑进行组织病理学检查,以及对74名具有不同人类白细胞抗原和家族史的患者的Hcrt、Hcrtr1和Hcrtr2进行突变筛查,来探究下丘脑分泌素在人类发作性睡病中的作用。在一例早发性发作性睡病患者中发现了一个Hcrt突变,该突变损害了肽的运输和加工。穹窿周区的原位杂交和肽放射免疫分析表明,在所有检查的人类病例中,下丘脑分泌素整体缺失,没有胶质细胞增生或炎症迹象。尽管下丘脑分泌素基因座对遗传易感性的贡献不大,但大多数人类发作性睡病病例与下丘脑分泌素系统缺陷有关。