Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly A Longitudinal Study

Rationale: Recent evidence suggests that obstructive sleep apnea (OSA) may be a risk factor for developing mild cognitive impairment and Alzheimer's disease. However, how sleep apnea affects longitudinal risk for Alzheimer's disease is less well understood. Objectives: To test the hypothes...

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Detalles Bibliográficos
Autores: Sharma, RA, Varga, AW, Bubu, OM, Pirraglia, E, Kam, K, Parekh, A, Wohlleber, M, Miller, MD, Andrade, A, Lewis, C, Tweardy, S, Buj, M, Yau, PL, Sadda, R, Mosconi, L, Li, Y, Butler, T, Glodzik, L, Fieremans, E, Babb, JS, Blennow, K, Zetterberg, H, Lu, SE, Badia, SG, Romero, S, Rosenzweig, I, Gosselin, N, Jean-Louis, G, Rapoport, D, de Leon, MJ, Ayappa, I, Osorio, RS
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2018
País:España
Institución:Institut d’Investigació Biomèdica Sant Pau (IIB Sant Pau)
Repositorio:r-IIB SANT PAU. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica Sant Pau
OAI Identifier:oai:iibsantpau.fundanetsuite.com:p3756
Acceso en línea:https://iibsantpau.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=3756
https://europepmc.org/articles/pmc6020410
Access Level:acceso abierto
Palabra clave:obstructive sleep apnea
amyloid burden
Pittsburgh compound B positron emission tomography scan
cerebrospinal fluid amyloid beta
cognitive impairment
Descripción
Sumario:Rationale: Recent evidence suggests that obstructive sleep apnea (OSA) may be a risk factor for developing mild cognitive impairment and Alzheimer's disease. However, how sleep apnea affects longitudinal risk for Alzheimer's disease is less well understood. Objectives: To test the hypothesis that there is an association between severity of OSA and longitudinal increase in amyloid burden in cognitively normal elderly. Methods: Data were derived from a 2-year prospective longitudinal study that sampled community-dwelling healthy cognitively normal elderly. Subjects were healthy volunteers between the ages of 55 and 90, were nondepressed, and had a consensus clinical diagnosis of cognitively normal. Cerebrospinal fluid amyloid beta was measured using ELISA. Subjects received Pittsburgh compound B positron emission tomography scans following standardized procedures. Monitoring of OSA was completed using a home sleep recording device. Measurements and Main Results: We found that severity of OSA indices (AHIall [F-1,F-88 = 4.26; P < 0.05] and AHI4%[F-1,F-87 = 4.36; P < 0.05]) were associated with annual rate of change of cerebrospinal fluid amyloid beta(42) using linear regression after adjusting for age, sex, body mass index, and apolipoprotein E4 status. AHIall and AHI4% were not associated with increases in AD(PiB)-mask (Alzheimer's disease vulnerable regions of interest Pittsburg compound B positron emission tomography mask) most likely because of the small sample size, although there was a trend for AHIall (F-1,F-28 = 2.96, P = 0.09; and F-1,F-28 = 2.32, not significant, respectively). Conclusions: In a sample of cognitively normal elderly, OSA was associated with markers of increased amyloid burden over the 2-year follow-up. Sleep fragmentation and/or intermittent hypoxia from OSA are likely candidate mechanisms. If confirmed, clinical interventions for OSA may be useful inpreventing amyloid build-up in cognitively normal elderly.