- Email: [email protected]
Alzheimer disease: sleep, orexin and cognitive decline
Sleep Medicine 14S (2013) e18–e92
Contents lists available at ScienceDirect
Sleep Medicine journal homepage: www.elsevier.com/locate/sleep
Abstracts for the 5th World Congress on Sleep Medicine, 28 September to 2 October 2013, Valencia, Spain Clinical and polysomnographic study of RBD in Parkinson’s disease from Egypt A. Mansour 1, T. Kamel 1, T. Asaad 2, Y. Metwally 1, H. Aref 1, N. Salah 1 1 Department of Neurology, Faculty of Medicine, Ain Shams University, Egypt 2 Department of Psychiatry, Faculty of Medicine, Ain Shams University, Egypt
Introduction: Patients with Parkinson’s disease (PD) are prone to sleep disturbances and disorders with a prevalence of 78–98% (Norlinah et al., 2009). The prevalence of RBD in idiopathic Parkinson’s disease varies from 15% to 58% (Iranzo et al., 2009).The importance of RBD is that it is now considered as an early marker of developing Parkinson’s disease (Arnulf, 2012). Objective: study the clinical and polysomnographic characteristics of PD patients with versus without RBD. Materials and methods: Thirty-six PD patients were enrolled from the Involuntary Movement outpatient clinic in Ain Shams University hospital and submitted to clinical assessment by UPDRS- III, Hamilton depression scale, structured sheet for sleep questionnaire, Mayo clinic sleep questionnaire to diagnose RBD, Pittsburgh sleep scale for sleep quality, Epwarth sleepiness scale to assess excessive day time sleepiness. In addition, REM sleep without atonia was assessed, in a one night video-polysomnography (PSG). Results: Thirteen patients (36%) were found to have RBD clinically and confirmed by PSG. RBD patients were of older age (p = 0.086), higher disease severity (p = 0.52), shorter disease duration (p = 0.108), there is was no difference between the RBD+ve group and RBD ve group as regard to tremors or rigidity as a predominant presentation. PSG analysis showed longer REM latency (p = 0.934), higher periodic leg movement index (PLMI) and respiratory disturbance index (RDI), p = 0.553, 0.198 respectively. Conclusion: Our findings support the association between RBD and PD as well as the clinical relevance of sleep disturbances in PD. Association with shorter disease duration may support that it is an early marker of the disease. http://dx.doi.org/10.1016/j.sleep.2013.11.007
Alzheimer disease: sleep, orexin and cognitive decline C. Liguori, A. Romigi, M. Albanese, S. Zannino, M. Marciani, F. Placidi Neuroscience Department, University Hospital of Rome Tor Vergata, Italy
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 P 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 (Ab1–42). 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. Ab1–42 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. http://dx.doi.org/10.1016/j.sleep.2013.11.008
Introduction: In Alzheimer’s disease (AD) several networks including regions regulating the sleep-wake rhythm are altered. Orexin-A http://dx.doi.org/10.1016/S1389-9457(13)01221-5
Contents lists available at ScienceDirect
Sleep Medicine journal homepage: www.elsevier.com/locate/sleep
Abstracts for the 5th World Congress on Sleep Medicine, 28 September to 2 October 2013, Valencia, Spain Clinical and polysomnographic study of RBD in Parkinson’s disease from Egypt A. Mansour 1, T. Kamel 1, T. Asaad 2, Y. Metwally 1, H. Aref 1, N. Salah 1 1 Department of Neurology, Faculty of Medicine, Ain Shams University, Egypt 2 Department of Psychiatry, Faculty of Medicine, Ain Shams University, Egypt
Introduction: Patients with Parkinson’s disease (PD) are prone to sleep disturbances and disorders with a prevalence of 78–98% (Norlinah et al., 2009). The prevalence of RBD in idiopathic Parkinson’s disease varies from 15% to 58% (Iranzo et al., 2009).The importance of RBD is that it is now considered as an early marker of developing Parkinson’s disease (Arnulf, 2012). Objective: study the clinical and polysomnographic characteristics of PD patients with versus without RBD. Materials and methods: Thirty-six PD patients were enrolled from the Involuntary Movement outpatient clinic in Ain Shams University hospital and submitted to clinical assessment by UPDRS- III, Hamilton depression scale, structured sheet for sleep questionnaire, Mayo clinic sleep questionnaire to diagnose RBD, Pittsburgh sleep scale for sleep quality, Epwarth sleepiness scale to assess excessive day time sleepiness. In addition, REM sleep without atonia was assessed, in a one night video-polysomnography (PSG). Results: Thirteen patients (36%) were found to have RBD clinically and confirmed by PSG. RBD patients were of older age (p = 0.086), higher disease severity (p = 0.52), shorter disease duration (p = 0.108), there is was no difference between the RBD+ve group and RBD ve group as regard to tremors or rigidity as a predominant presentation. PSG analysis showed longer REM latency (p = 0.934), higher periodic leg movement index (PLMI) and respiratory disturbance index (RDI), p = 0.553, 0.198 respectively. Conclusion: Our findings support the association between RBD and PD as well as the clinical relevance of sleep disturbances in PD. Association with shorter disease duration may support that it is an early marker of the disease. http://dx.doi.org/10.1016/j.sleep.2013.11.007
Alzheimer disease: sleep, orexin and cognitive decline C. Liguori, A. Romigi, M. Albanese, S. Zannino, M. Marciani, F. Placidi Neuroscience Department, University Hospital of Rome Tor Vergata, Italy
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 P 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 (Ab1–42). 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. Ab1–42 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. http://dx.doi.org/10.1016/j.sleep.2013.11.008
Introduction: In Alzheimer’s disease (AD) several networks including regions regulating the sleep-wake rhythm are altered. Orexin-A http://dx.doi.org/10.1016/S1389-9457(13)01221-5