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Evidence of Neurodegeneration in Obstructive Sleep Apnea: Relationship Between Obstructive Sleep Apnea and Cognitive Dysfunction in the Elderly

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Evidence of Neurodegeneration in Obstructive Sleep Apnea: Relationship Between Obstructive Sleep Apnea and Cognitive Dysfunction in the Elderly Journal of Neuroscience Research 93:1778–1794 (2015) Review Evidence of Neurodegeneration in Obstructive Sleep Apnea: Relationship Between Obstructive Sleep Apnea and Cognitive Dysfunction in the Elderly Mak Adam Daulatzai* Sleep Disorders Group, EEE/Melbourne School of Engineering, The University of Melbourne, Parkville, Victoria, Australia The incidence of dementia and obstructive sleep apnea There are two major types of sleep-disordered (OSA) increases with age. Late-onset Alzheimer’s disease breathing (SDB), obstructive sleep apnea (OSA) and cen- (AD) is an irreversible neurodegenerative disease of the tral sleep apnea (CSA). Among the two types of sleep elderly characterized by amyloid b (Ab) plaques and neu- apneas, OSA is the most common type, constituting rofibrillary tangles. The disease involves widespread syn- greater than 85% of all cases of SDB; CSA is far less com- aptic loss in the neocortex and the hippocampus. Rodent mon (Morgenthaler et al., 2006) People with untreated and clinical studies suggest that OSA impairs the struc- OSA stop breathing repeatedly during their sleep because tural integrity of several brain regions, including the of recurrent collapse of the upper airway with inspiration, medial temporal lobe. Indeed, hypoxia, hypertension, resulting in apnea, intermittent hypoxia (IH), oxygen hypoperfusion, endothelial dysfunction, inflammation, desaturation, and arousal from sleep (Guilleminault et al., and oxidative stress noted in OSA patients also occur in 1976). Generally, an apnea in adults is defined by a >90% AD patients. This Review highlights pathological com- decrease in respiratory airflow for 10 or more sec; how- monality, showing that OSA upregulates Ab, tau hyper- ever, there need not be a complete cessation of airflow. phosphorylation, and synaptic dysfunction. Indeed, OSA and hypertension trigger hypoperfusion and hypometab- SIGNIFICANCE: olism of brain regions, including cortex and hippocam- pus. Several studies show that hypertension-driven brain Obstructive sleep apnea (OSA) can significantly affect physical and damage and pathogenic mechanisms lead to an Ab mental health, including cognitive health. OSA induces neurodege- increase. The pathophysiological mechanism by which nerative changes resulting from two of its main and integral processes, OSA enhances hypertension may be linked to sympa- intermittent hypoxia and sleep fragmentation. Because of the patho- thoexcitation, oxidative stress, and endothelial dysfunc- logical impact of hypoxia vis-a-vis hypertension, hypoperfusion, tion. Strong pathophysiological similarities that exist impaired glucose metabolism, and adverse cardiovascular, neurocircu- between OSA and AD are underscored here. For exam- latory, and metabolic consequences, amyloid b generation and tau ple, the hippocampus is negatively impacted in both OSA phosphorylation are upregulated, leading to memory/cognitive impairment and progression to Alzheimer’s disease (AD). Further- and AD. OSA promotes hippocampal atrophy, which is more, OSA-related inflammation and oxidative stress impair synaptic associated with memory impairment. Cognitive impair- function and neural circuitry, leading to a decline in neuronal func- ment, even in the absence of manifest dementia, is an tion in several key brain areas and, thus, inducing cognitive decline. important independent predictor of mortality. However, Sustained OSA-promoted cognitive dysfunction overlaps with that several pathophysiological mechanisms in OSA are noted in AD-associated cognitive impairment. reversible with appropriate therapy. OSA, therefore, is a modifiable risk factor of cognitive dysfunction, and treat- ing OSA prior to mild cognitive impairment may be an *Correspondence to: Mak Adam Daulatzai, MSc, PhD, MD, Senior effective prevention strategy to reduce risk for cognitive Medical Research Fellow, Sleep Disorders Group, EEE/Melbourne decline and AD in middle-aged persons and the elderly. School of Engineering, The University of Melbourne, 3rd Floor, Room 344, Parkville, Victoria 3010, Australia. E-mail: [email protected] VC 2015 Wiley Periodicals, Inc. Received 29 May 2015; Revised 2 August 2015; Accepted 4 August Key words: Alzheimer’s disease; obstructive sleep 2015 apnea; hypoperfusion; neuroinflammation; Abeta; tau Published online 24 August 2015 in Wiley Online Library hyperphosphorylation; cognitive dysfunction (wileyonlinelibrary.com). DOI: 10.1002/jnr.23634 VC 2015 Wiley Periodicals, Inc. OSA and Neuropathogenesis of Late-Onset Alzheimer’s Disease 1779 Hypopnea is defined as a 50% decrease in nasal airflow prevalence in those who are institutionalized (Ancoli- with a 4% oxygen desaturation (Ward et al., 2013). Israel et al., 1991a). Unfortunately, few interventions Apneas and hypopneas have similar pathophysiology. (behavioral or pharmacological) effectively delay progres- SDB is defined as apnea–hypopnea index (AHI) 5/hr sion in cognitive decline or improve memory and quality with symptoms or 15/hr with/without symptoms. Dif- of life for AD patients. ferent hypopnea scoring rules can significantly influence Atrophy, degeneration, and progressive loss of neu- the AHI and diagnosis of SDB (Ward et al., 2013; Hein- rons (referred to here as neurodegeneration) are prominent rich et al., 2015). For example, using the American Acad- in neurodegenerative diseases, including AD, Parkinson’s emy of Sleep Medicine (AASM; 2007) recommended disease, amyotrophic lateral sclerosis, Creutzfeldt-Jakob definition may lead to a lower AHI and less OSA severity disease, and Huntington’s disease. The outstanding risk compared with the previous standard (BaHammam et al., factor for developing neurodegenerative diseases, and cer- 2014; Nixon et al., 2014). The AASM definition for hypo- tainly AD, is aging. The characteristic neuropathological pneas is somewhat liberal, so it may lead to a higher AHI, lesions in AD are senile plaques formed by amyloid b with inclusion of less severe events. A discussion of differ- (Ab) and located outside neurons and neurofibrillary tan- ent published hypopnea definitions and the implications of gles (NFTs) comprising abnormally hyperphosphorylated revised AASM rules on scoring apneic and hypopneic tau protein and located within neurons (Su et al., 1996; respiratory events is beyond the scope of this Review. Zhao et al., 2010). Ab is considered to be the noxious eti- Interested readers should consult appropriate articles on ological agent (as per the amyloid cascade hypothesis) that this topic (Thornton et al., 2012; Shahar, 2014). may trigger synaptopathy, glial (including microglial and Recent estimates suggest that up to 30% of men and astrocytic) activation-related inflammatory response, neu- 12% of women between 30 and 70 years of age are ronal ionic dyshomeostasis, oxidative damage, tau hyper- affected by OSA (Peppard et al., 2013). The prevalence phosphorylation (because of altered activities of relevant estimates of moderate-to-severe SDB (AHI 15 events/ kinases and phosphatases), and eventual neuronal death hr) were studied in different age groups. These estimates (De Felice et al., 2007). In neurofibrillary degeneration were 10% among 30–49-year-old men, 17% among 50– pathology, hyperphosphorylated tau protein accumulates 70-year-old men, 3% among 30–49-year-old women, in neurons as paired helical filaments in NFTs, induces and 9% among 50–70-year-old women (Peppard et al., abnormal cellular metabolism, and causes neuronal death. 2013). A polysomnographic study of 2,911 older men NFTs are associated with memory and cognitive dysfunc- 6 (76.38 5.53 years of age) conducted by Ancoli-Israel tions (Goedert, 1993; Wes et al., 2014). and colleagues found prevalence of moderate-to-severe AD pathology starts years or decades prior to clinical SDB to be 21.4–26.4% (Mehra et al., 2007). diagnosis. This Review focuses on the significance of Some of the long-term health problems associated with untreated OSA include hypertension, stroke, diabe- OSA-related IH signaling and upregulation of differing tes, cardiac arrhythmias, myocardial infarction, heart fail- pathophysiological mechanisms, including hypertension, ure, and depression (Daulatzai, 2013a). OSA has been endothelial dysfunction, hypoperfusion, glucose dysho- extensively reviewed elsewhere (Ryan and Bradley, 2005; meostasis, inflammation, oxidative stress, and neurotoxic- White, 2005; Daulatzai, 2013a). Currently, the standard ity. These are posited to trigger memory and cognitive therapeutic option for the management of OSA is contin- dysfunction prior to frank AD. This Review underscores uous positive airway pressure (CPAP). CPAP provides a OSA-related evidence relevant to AD and emphasizes a continuous, stable, predetermined pressure of air that link between the role of OSA in triggering neuronal ameliorates negative pressure and keeps the upper airway pathology (dysfunction and degeneration) and the possible from collapsing. pathogenesis of cognitive dysfunction in AD. Alzheimer’s disease (AD) is the most common neu- PREVALENCE OF OSA IN THE ELDERLY rodegenerative disorder affecting the elderly and is an escalating public health issue. During the early stages of Advancing age is characterized by a decline in physiologi- disease, sleep disturbances and forgetfulness are generally cal functions. It is a complex state, characterized by the first presenting symptoms (Pace-Schott and Spencer, accumulation of pathology (Federal Interagency Forum 2015). AD is characterized by progressive and gradual on Aging Related Statistics, 2010). Consequently,
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