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      Obstructive sleep apnoea and Alzheimer’s disease: In search of shared pathomechanisms

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          Highlights

          • Alzheimer’s disease (AD) is a significant public health concern.

          • The processes involved in the pathogenesis of AD are shown to overlap with those found in cognitive decline in Obstructive Sleep Apnoea (OSA).

          • An excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA.

          • External factors, such are systemic inflammation and obesity, can interfere with immunological processes of the brain, and promote disease progression.

          Abstract

          Alzheimer’s disease (AD) is a significant public health concern. The incidence continues to rise, and it is set to be over one million in the UK by 2025. The processes involved in the pathogenesis of AD have been shown to overlap with those found in cognitive decline in patients with Obstructive Sleep Apnoea (OSA). Currently, the standard treatment for OSA is Continuous Positive Airway Pressure. Adherence to treatment can, however, be an issue, especially in patients with dementia. Also, not all patients respond adequately, necessitating the use of additional treatments. Based on the body of data, we here suggest that excessive and prolonged neuronal activity might contribute to genesis and acceleration of both AD and OSA in the absence of appropriately structured sleep. Further, we argue that external factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain, and further promote disease progression. If this hypothesis is proven in future studies, it could have far-reaching clinical translational implications, as well as implications for future treatment strategies in OSA.

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          Most cited references50

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          Alzheimer's disease.

          Alzheimer's disease is the most common cause of dementia. Research advances have enabled detailed understanding of the molecular pathogenesis of the hallmarks of the disease--ie, plaques, composed of amyloid beta (Abeta), and tangles, composed of hyperphosphorylated tau. However, as our knowledge increases so does our appreciation for the pathogenic complexity of the disorder. Familial Alzheimer's disease is a very rare autosomal dominant disease with early onset, caused by mutations in the amyloid precursor protein and presenilin genes, both linked to Abeta metabolism. By contrast with familial disease, sporadic Alzheimer's disease is very common with more than 15 million people affected worldwide. The cause of the sporadic form of the disease is unknown, probably because the disease is heterogeneous, caused by ageing in concert with a complex interaction of both genetic and environmental risk factors. This seminar reviews the key aspects of the disease, including epidemiology, genetics, pathogenesis, diagnosis, and treatment, as well as recent developments and controversies.
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            Adult obstructive sleep apnoea.

            Obstructive sleep apnoea is an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen desaturation and disrupted sleep. Features include snoring, witnessed apnoeas, and sleepiness. Pathogenesis varies; predisposing factors include small upper airway lumen, unstable respiratory control, low arousal threshold, small lung volume, and dysfunctional upper airway dilator muscles. Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy, and smoking. Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemic hypertension. It has also been linked to myocardial infarction, congestive heart failure, stroke, and diabetes mellitus though not definitively. Continuous positive airway pressure is the treatment of choice, with adherence of 60-70%. Bi-level positive airway pressure or adaptive servo-ventilation can be used for patients who are intolerant to continuous positive airway pressure. Other treatments include dental devices, surgery, and weight loss.
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              Obstructive sleep apnoea syndrome.

              Obstructive sleep apnoea syndrome (OSAS) is a common clinical condition in which the throat narrows or collapses repeatedly during sleep, causing obstructive sleep apnoea events. The syndrome is particularly prevalent in middle-aged and older adults. The mechanism by which the upper airway collapses is not fully understood but is multifactorial and includes obesity, craniofacial changes, alteration in upper airway muscle function, pharyngeal neuropathy and fluid shift towards the neck. The direct consequences of the collapse are intermittent hypoxia and hypercapnia, recurrent arousals and increase in respiratory efforts, leading to secondary sympathetic activation, oxidative stress and systemic inflammation. Excessive daytime sleepiness is a burden for the majority of patients. OSAS is also associated with cardiovascular co-morbidities, including hypertension, arrhythmias, stroke, coronary heart disease, atherosclerosis and overall increased cardiovascular mortality, as well as metabolic dysfunction. Whether treating sleep apnoea can fully reverse its chronic consequences remains to be established in adequately designed studies. Continuous positive airway pressure (CPAP) is the primary treatment modality in patients with severe OSAS, whereas oral appliances are also widely used in mild to moderate forms. Finally, combining different treatment modalities such as CPAP and weight control is beneficial, but need to be evaluated in randomized controlled trials. For an illustrated summary of this Primer, visit: http://go.nature.com/Lwc6te.
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                Author and article information

                Contributors
                Journal
                Neurosci Biobehav Rev
                Neurosci Biobehav Rev
                Neuroscience and Biobehavioral Reviews
                Pergamon Press
                0149-7634
                1873-7528
                1 March 2018
                March 2018
                : 86
                : 142-149
                Affiliations
                [a ]Sleep and Brain Plasticity Centre, CNS, IoPPN, King’s College London, UK
                [b ]Croatian Institute for Brain Research, Medical School, University of Zagreb, Croatia
                [c ]Sleep Disorders Centre, Guy’s and St Thomas’ Hospital, London, UK
                [d ]Department of Neuroimaging, IoPPN, King’s College London, UK
                [e ]Surrey Sleep Research Centre, Department of Clinical and Experimental Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK
                [f ]Department of Neurology, Guy’s and St Thomas’ Hospital, London, UK
                [g ]Academic Unit of Sleep and Breathing, National Heart and Lung Institute, Imperial College London, UK and NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London, UK
                Author notes
                [* ]Corresponding author at: Sleep and Brain Plasticity Centre, CNS, IoPPN, King’s College London, UK. ivana.1.rosenzweig@ 123456kcl.ac.uk
                [1]

                Joint first authorship.

                Article
                S0149-7634(17)30435-9
                10.1016/j.neubiorev.2017.12.004
                6562163
                29223769
                d640f48e-fbaa-4342-ac7d-6b163c658a1c
                © 2017 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 14 June 2017
                : 29 October 2017
                : 4 December 2017
                Categories
                Article

                Neurosciences
                obstructive sleep apnea,alzheimer’s disease,neuroinflammation,astrocytes
                Neurosciences
                obstructive sleep apnea, alzheimer’s disease, neuroinflammation, astrocytes

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