CSF beta‐amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?. (19th February 2014)

• Record Type: Journal Article
• Authors: Liguori, Claudio; Placidi, Fabio; Albanese, Maria; Nuccetelli, Marzia; Izzi, Francesca; Marciani, Maria Grazia; Mercuri, Nicola Biagio; Bernardini, Sergio; Romigi, Andrea
• Is Part Of: Journal of sleep research. Volume 23:Number 4(2014:Dec.)
• Page Start: 420
• Page End: 424
• Publication Date: 2014-02-19
• Subjects: Sleep -- Periodicals; Sleep disorders -- Periodicals; 612.821
• DOI: 10.1111/jsr.12130
• Languages: English
• ISSNs: 0962-1105

Abstract

<abstract abstract-type="main" id="jsr12130-abs-0001"> <title>Summary</title> <p>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‐amyloid_1–42 and/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta‐amyloid_1–42 CSF levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of CSF beta‐amyloid_1–42 (&lt;500 pg mL⁻¹) in six of 16 narcoleptic patients (37.5%). We hypothesize that the significant decrease of the CSF beta‐amyloid_1–42 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.</p> </abstract>