Lipocalin-type prostaglandin D synthase levels increase in patients with narcolepsy and idiopathic hypersomnia

Author:

Wang Peipei12,Li Qinghua1,Dong Xiaosong1,An Haiyan3,Li Jing1,Zhao Long1,Yan Han1,Aritake Kosuke4,Huang Zhili5ORCID,Strohl Kingman P6,Urade Yoshihiro7,Zhang Jun8,Han Fang1ORCID

Affiliation:

1. Department of Pulmonary Medicine, Peking University People’s Hospital, Beijing, China

2. Sleep and Psychosomatic Medicine Center, The Third People’s Hospital of Hainan Province, Sanya, Hainan, China

3. Department of Anesthesia, Peking University People’s Hospital, Beijing, China

4. Laboratory of Chemical Pharmacology, Daiichi University of Pharmacy, Minami-ku, Fukuoka, Japan

5. Department of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, and Institutes of Brain Science, Fudan University, Shanghai, China

6. Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Case Western Reserve University, and Cleveland Louis Stokes VA Medical Center, Cleveland, OH

7. Isotope Science Center, The University of Tokyo, Bunkyo-ku, Tokyo, Japan

8. Department of Neurology, Peking University People’s Hospital, Beijing, China

Abstract

Abstract Study Objectives Excessive daytime sleepiness (EDS) is a frequent cause for consultation and a defining symptom of narcolepsy and idiopathic hypersomnia (IH). The associated mechanisms remain unclear. Lipocalin-type prostaglandin D synthase (LPGDS) is a plausible sleep-inducing candidate. This study is to compare cerebral spinal fluid (CSF) and serum LPGDS levels in patients group with hypersomnia of central origin, including those with narcolepsy type 1 (NT1) and type 2 (NT2) and IH, to those in healthy controls (Con). Methods Serum LPGDS, CSF LPGDS, and CSF hypocretin-1(Hcrt-1) levels were measured by ELISA in 122 narcolepsy patients (106 NT1 and 16 NT2), 27 IH, and 51Con. Results LPGDS levels in CSF (p = 0.02) and serum (p < 0.001) were 22%–25% lower in control subjects than in patients with EDS complaints, including NT1, NT2, and IH. In contrast to significant differences in CSF Hcrt-1 levels, CSF L-PGDS levels and serum L-PGDS were comparable among NT1, NT2, and IH (p > 0.05), except for slightly lower serum LPGDS in IH than in NT1 (p = 0.01). Serum L-PGDS correlated modestly and negatively to sleep latency on MSLT (r = −0.227, p = 0.007) in hypersomnia subjects. Conclusions As a somnogen-producing enzyme, CSF/serum LPGDS may serve as a new biomarker for EDS of central origin and imply a common pathogenetic association, but would complement rather than replaces orexin markers.

Funder

NSFC

JSPS

Publisher

Oxford University Press (OUP)

Subject

Physiology (medical),Neurology (clinical)

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