CSF beta-amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?

Abstract

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-amyloid1-42 and/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta-amyloid1-42 CSF levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of CSF beta-amyloid1-42 (<500 pg mL(-1) ) in six of 16 narcoleptic patients (37.5%). We hypothesize that the significant decrease of the CSF beta-amyloid1-42 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.

DOI: 10.1111/jsr.12130
0501002014201520162017
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@article{Liguori2014CSFBL, title={CSF beta-amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?}, author={Claudio Liguori and Fabio Placidi and Maria Albanese and Marzia Nuccetelli and Francesca Izzi and Maria Grazia Marciani and Nicola Biagio Mercuri and Sergio Bernardini and Andrea Romigi}, journal={Journal of sleep research}, year={2014}, volume={23 4}, pages={420-4} }