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• W2030334368 abstract "Introduction In Alzheimer’s disease (AD) several networks including regions regulating the sleep-wake rhythm are altered. Orexin-A is an hypothalamic neuropeptide contributing to the regulation of the sleep-wake cycle. The aim of our study was to investigate the possible involvement of the orexinergic system in the AD neurodegenerative processes and its relationship with sleep impairment. Materials and methods We included 48 consecutive untreated AD patients and 29 healthy controls. Based on MMSE, AD patients were divided in 2 groups: mild AD (MMSE  ⩾  21; 21 subjects) and moderate-severe AD (MMSE   21; 27 subjects). We quantified orexin CSF levels in AD patients and controls, and examined potential links to the established AD markers CSF levels, as tau, phospho-tau (ptau), and beta-amyloid1–42 (A β 1–42). Moreover, AD patients underwent a full nocturnal polysomnography (PSG). Finally, CSF results were correlated with sleep structure parameters and MMSE. Results Regarding CSF data, control subjects showed orexin CSF levels not significantly different with AD patients as well as with mild AD subjects. However, moderate-severe AD patients showed increased orexin CSF levels in respect to both mild AD patients and controls. Regarding PSG parameters, moderate–severe AD patients, compared to mild AD subjects, showed a significant reduction in sleep efficiency (SE) and a significant increase in wakefulness after sleep onset (WASO) and in REM latency. Moreover, in AD patients the orexin CSF levels were negatively correlated with REM sleep, slow wave sleep (SWS) and SE, whereas were positively correlated with WASO and sleep latency. Furthermore, it appeared to exist a positive correlation between the increase of orexin and tau CSF levels in AD patients. A β 1–42 CSF levels were negatively correlated with WASO whereas were positively correlated with REM sleep. Tau CSF levels were negatively correlated with SWS. The decrease of MMSE correlated with the impairment of SE and REM sleep and the increase of WASO. Conclusion Our study shows that in AD cognitive decline is linked to a parallel sleep deterioration, which appears to be related to an increase of the CSF orexin levels. In conclusion, our results demonstrate that the orexinergic system is not impaired in AD, but its output and function appears to be overexpressed along the progression of neurodegenerative processes, possibly due to an unbalance of the neurotransmitters networks regulating the wake-sleep cycle towards the systems promoting wakefulness. Acknowledgements We are grateful to Ms. Alessandra Nitti for technical support, Dr. Francesca Izzi for acquisition of data, Prof. Nicola Biagio Mercuri for study supervision and Prof. Giuseppe Sancesario and Dr. Alessandro Martorana for acquisition of data and study supervision." @default.
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• W2030334368 date "2013-12-01" @default.
• W2030334368 modified "2023-10-12" @default.
• W2030334368 title "Alzheimer disease: sleep, orexin and cognitive decline" @default.
• W2030334368 doi "https://doi.org/10.1016/j.sleep.2013.11.008" @default.
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