The aging process tends to promote an overall increase in inflammation compromising the immunologic system regulation, sleep/wakefulness pattern, and neurocognitive performance. In elders, there is an increase in repetitive arousals during sleep, secondary to breathing interruption by pharynx collapse, generating a transient reduction in oxygen delivery to the brain known as obstructive sleep apnea. This lack in oxygen supply results in an inflammatory process producing brain damage. Some substances present in the blood seem to be associated to neurocognitive damage, like S100β protein, cortisol, interleukin 1-β,6 and TNF-α. In the other way, a substance called brain-derived neurotrophic factor (BDNF) enhances cognitive function, and memory consolidation improvement.

An intermittent hypoxia in obstructive sleep apnea induces the production of reactive oxygen species (ROS), oxidative damage and inflammation generating pro-inflammatory cytokines, reactive gliosis and neuronal damage. The increase in oxidative damage seems to be associated to age, contributing to the progress of neurodegeneration. Transient hypoxemia leads to autonomic excitation causing hyperactivity of the sympathetic nervous system (SNS), and activation of the hypothalamic-pituitary-adrenal (HPA) axis, causing immunological changes and increased risk of damage to mental functions. Night awakenings caused by OSA are associated with changes on the HPA axis, resulting in increased serum cortisol levels. The fluctuation in serum cortisol levels at night is intrinsically related to sleep, and increases with advancing age. BDNF is responsible for increasing the growth of neurites, and synaptogenesis, preventing programmed cell death in adults, and is involved in stress responses on the HPA axis. Low BDNF levels are associated to cognitive impairment, less memory consolidation, depression, and OSA. There is a positive correlation between levels of BDNF and cortisol related to physiological regulation of brain activities. The increase in oxidative damage caused by intermittent hypoxia during obstructive sleep apnea increases serum levels of the s100β protein promoting reactive gliosis or astrogliosis being associated to depression in the elderly. Obstructive sleep apnea syndrome is associated with development of cardiovascular and neurological diseases by activating pro-inflammatory pathways. However, in elderly individuals, regardless of other specific pathologies, they already have a pro-inflammatory state secondary to loss of regulation of the immune system.

Inclusion criteria:

• Individuals aged 65 to 80;
• both sexes;
• free and informed consent form previously signed for participation in the MEDIDAS cohort study;
• previous performance of outpatient polysomnography with adequate technical quality
• AHI ≤ 5 or ≥ 30 events/hour;
• previous blood collection between 7-9 am; questionnaires.

Exclusion criteria:

• Have had treatment for sleep apnea;
• suffer from rheumatic or chronic diseases such as diabetes mellitus, heart failure, coronary artery disease, chronic renal failure or nephropathy (creatinine> 1.8 mg / dL), liver disease, history of stroke, aortic aneurysm, marked elevation in blood arterial pressure (> 180/110 mmHg), assessed by 24-hour ambulatory blood pressure monitoring (ABPM);
• cognitive deficit verified in the Mini Mental State Examination;
• diagnosis of Alzheimer's and Parkinson's.

A sample will be composed from the database and the biorepository of volunteers participating in the MEDIDAS cohort study. The database was stored in the Non-Invasive Methods Unit (UMNI) and the biorepository of blood aliquots initiated at -80ºC in the Molecular and Protein Analysis Unit (UAMP) in Hospital de Clínicas de Porto Alegre, Brazil. All data and aliquots will not suffer any type of intervention in the studies of the MEDIDAS cohort.