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P4‐224: Alzheimer’s Disease Patients With Osas History Have Higher CSF Tau Levels
Author(s) -
Hooghiemstra Astrid M.,
Visser Pieter Jelle,
Slot Rosalinde E.R.,
Teunissen Charlotte E.,
Scheltens Philip,
van der Flier Wiesje M.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.06.2316
Subject(s) - obstructive sleep apnea , medicine , dementia , cohort , cognitive decline , disease , gastroenterology , cerebrospinal fluid , sleep apnea , alzheimer's disease , hypoxia (environmental) , medical history , chemistry , organic chemistry , oxygen
Background: Obstructive sleep apnea syndrome (OSAS) occurs more frequently in Alzheimers disease (AD) than in controls. OSAS is characterized by the obstruction of the upper airway resulting in nocturnal intermittent hypoxia. Hypoxia has been found to be related to the Alzheimer biomarkers amyloid-beta and tau in animal studies. The aim of the present study was to investigate whether a history of OSAS is associated with cerebrospinal fluid (CSF) levels of amyloid-beta 42 (AB42), total tau (tau) and phosphorylated tau (ptau) in patients with subjective cognitive decline (SCD), mild cognitive impairment (MCI), and AD. Methods:We included 59 patients who reported OSAS in their medical history (age 63 (8) years, 11 (19%) female; 14 AD, 15 MCI, 30 SCD) from the Amsterdam Dementia Cohort. We matched these patients for baseline diagnosis, gender, age, and year of evaluation, on a 1:2 basis to patients without an OSAS history (N1⁄4118). CSFAB42, tau and ptau were assessed using ELISA (Innotest). We assessed the association between OSAS and the CSF biomarkers with Linear Mixed Models (LMM), that included terms for OSAS, diagnosis, and the interactions between OSAS and diagnosis. All models were adjusted for APOE E4 status. Results:In the total sample there was no association between OSAS and CSF biomarkers. The relationship between OSAS and tau tended to be different between diagnostic groups (p-value interaction .095). Post-hoc analysis showed that AD patients with a history of OSAS had higher tau levels than those without OSAS (estimated mean [95% CI]: 845 [715-976] vs. 647 [549-744] pg/ml, p-value 1⁄4 .02). OSAS was not associated with tau in SCD and MCI patients. There was no interaction between OSAS and diagnosis for CSF AB42 and ptau. Conclusions:We found that a history of OSAS is associated with higher CSF tau levels in AD. These findings could fit with the idea that hypoxia might have an additive effect to neuronal injury in AD, or vice versa, that patients with high tau levels are at increased risk of OSAS. However, inferences on causal relationships cannot be made given the observational nature of the study.