A review of inflammatory effects of sleep deprivation on cognitive processes in Alzheimer's disease
A review of inflammatory effects of sleep deprivation on cognitive processes in Alzheimer's disease
Morteza Nazari Khiji,1,*Maryam poorsaadat,2
1. Student Research Committee, Sabzevar University of Medical Sciences, Sabzevar, Iran 2. Student Research Committee, Sabzevar University of Medical Sciences, Sabzevar, Iran
Introduction: Sleep disturbances, one of the characteristic symptoms of Alzheimer's disease (AD), has been proven is related to the pathophysiology of AD and can influence the cognitive functions in patients with AD. Sleep deprivation has been reported to be associated with inflammation. Evidence links neuroinflammation to cognitive deficits in AD. In this paper, we aimed to discuss the role of inflammation as a consequence of sleep deprivation in Alzheimer's progression and declining cognitive functions.
Methods: A search was conducted on PubMed, Cochrane Library, and Web of Science databases from 2010 to 2022 using the terms "sleep deprivation", "Alzheimer's disease", "cognition" and "inflammation".
Results: AD, the most common type of dementia, is characterized by the progressive loss of neurons, which typically leads to severe impairments in cognitive functions including memory and learning. There is a great deal of evidence suggesting Neuroinflammation as main part of the pathological progression of AD, but the molecular mechanisms are still not clear. Sleep deprivation has been associated with a chronic inflammatory state leading to inflammatory pathologies, including neurodegenerative diseases. Findings from sleep deprivation studies indicate that sleep deprivation is associated with increases in cytokines such as IL-1, IL-6, IL-17, IL-1β and TNF and induces an activation of vascular endothelial markers (i.e. E-selectin, s-intercellular adhesion molecule, s-ICAM-1). Interestingly, among people with chronic sleep deprivation, it appears that vulnerability to inflammation is increased after an episode of sleep loss. Also, sleep loss induces a systemic inflammation characterized by the release of several molecules, such as cytokines, chemokines, and acute-phase proteins; all of them may lead to changes in cellular components of the blood-brain barrier and induces blood-brain barrier disruption. Raised serum pro-inflammatory cytokines have been associated with a cognitive decline in Alzheimer's disease.
Conclusion: Taken together, sleep deprivation has been shown to cause neurocognitive impairment such as impaired memory and learning. Inflammatory processes may be an important biological mechanism linking deprivative sleep to cognitive impairment and should be considered as a risk factor for developing and progressing Alzheimer's disease. Hence, the correction of sleep deprivation could be a preventive agent of severe cognitive decline in patients with Alzheimer's disease.