Abstract
Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by repeated episodes of upper airways collapse during the sleep. The following intermittent hypoxia triggers a state of chronic inflammation, which also interests the nervous system leading to neuronal damage and increased risk of cognitive impairment. Brain derived neurotrophic factor (BDNF) is a growth factor often associated with neuroplasticity and neuroprotection whose levels increase in several condition associated with neuronal damage. However, whether patients affected by OSAS have altered BDNF levels and whether such alteration may be reflective of their cognitive impairment is still controversial. Here we show that, when compared to healthy control volunteers, OSAS patients have increased serum levels of BDNF. Moreover, OSAS patients with the higher levels of BDNF also have reduced neurocognitive impairment as measured by The Montreal Cognitive Assessment (MoCA) questionnaire. Treatment with standard non-invasive mechanical ventilation (CPAP) also was able to ameliorate the level of cognitive impairment. Altogether our results indicate that BDNF levels represent a neuroprotective response to intermittent hypoxia in OSAS patients.
Highlights
Obstructive sleep apnea syndrome (OSAS) is a common sleep disorder characterized by repeated episodes of partial or total collapse of the upper airways which result in chronic intermittent hypoxia (CIH), sleep fragmentation, hypercapnia and sympathetic hyperactivity [1]
Subjects with OSAS had a median age of 61.9 ± 10.5 years, a mean body mass index (BMI) of 32.9 ± 6.9, a mean abdomen circumference of 118.2 ± 15.6 cm, and an average neck circumference of 44.4 ± 3.5 cm
Whether Brain derived neurotrophic factor (BDNF) levels are elevated in OSAS, a pathological condition characterized by intermittent hypoxia, is still controversial
Summary
Obstructive sleep apnea syndrome (OSAS) is a common sleep disorder characterized by repeated episodes of partial or total collapse of the upper airways which result in chronic intermittent hypoxia (CIH), sleep fragmentation, hypercapnia and sympathetic hyperactivity [1]. Neurocognitive impairment is one of the major complications associated with OSAS which represents a common comorbidity for patients affected by neurodegenerative disease such as Alzheimer and Parkinson [2, 3]. Sleep fragmentation may partially contribute to cognitive dysfunction, the majority of experimental and clinical evidences indicate that CIH is mainly responsible for the functional and structural brain alterations beyond cognitive.
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