{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T17:35:41Z","timestamp":1790962541459,"version":"4.1.0"},"reference-count":20,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,2,19]],"date-time":"2014-02-19T00:00:00Z","timestamp":1392768000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Sleep Research"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Narcolepsy is characterized by hypocretin deficiency due to the loss of hypothalamic orexinergic neurons, and is associated with both the human leucocyte antigen <jats:styled-content style=\"fixed-case\">DQB<\/jats:styled-content>1*06:02 and the <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> 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 (<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>) levels of beta\u2010amyloid<jats:sub>1\u201342<\/jats:sub> and\/or total tau proteins in a sample of narcoleptic patients, we analysed 16 narcoleptic patients and 16 healthy controls. Beta\u2010amyloid<jats:sub>1\u201342<\/jats:sub> <jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> levels were significantly lower in narcoleptic patients compared with healthy controls. We also documented pathologically low levels of <jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> beta\u2010amyloid<jats:sub>1\u201342<\/jats:sub> (&lt;500\u00a0pg\u00a0mL<jats:sup>\u22121<\/jats:sup>) in six of 16 narcoleptic patients (37.5%). We hypothesize that the significant decrease of the <jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> beta\u2010amyloid<jats:sub>1\u201342<\/jats:sub> levels in narcoleptic patients may support both the inflammatory\/autoimmune hypothesis as the basis of the pathogenesis of narcolepsy and the prevalence of an \u2018amyloidogenic\u2019 pathway caused by the deficiency of the alpha\u2010secretases enzymes.<\/jats:p>","DOI":"10.1111\/jsr.12130","type":"journal-article","created":{"date-parts":[[2014,2,20]],"date-time":"2014-02-20T09:08:32Z","timestamp":1392887312000},"page":"420-424","source":"Crossref","is-referenced-by-count":43,"title":["<scp>CSF<\/scp> beta\u2010amyloid levels are altered in narcolepsy: a link with the inflammatory hypothesis?"],"prefix":"10.1111","volume":"23","author":[{"given":"Claudio","family":"Liguori","sequence":"first","affiliation":[{"name":"Department of Systems Medicine Neurophysiopathology Unit Sleep Medicine Centre University of Rome 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