Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly A Longitudinal Study
Por:
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
Publicada:
1 abr 2018
Resumen:
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.
Filiaciones:
Sharma, RA:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Varga, AW:
Icahn Sch Med Mt Sinai, Div Pulm Crit Care & Sleep Med, New York, NY 10029 USA
Bubu, OM:
Univ S Florida, Dept Epidemiol & Biostat, Coll Publ Hlth, Tampa, FL USA
Pirraglia, E:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Kam, K:
Icahn Sch Med Mt Sinai, Div Pulm Crit Care & Sleep Med, New York, NY 10029 USA
Parekh, A:
Univ Iowa, Coll Engn, Iowa City, IA 52242 USA
Wohlleber, M:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Miller, MD:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Andrade, A:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Lewis, C:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Tweardy, S:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Buj, M:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Yau, PL:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Sadda, R:
Columbia Univ, Med Ctr, Harlem Hosp, New York, NY USA
Mosconi, L:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Li, Y:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Butler, T:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Glodzik, L:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Fieremans, E:
NYU, Dept Radiol, Sch Med, Ctr Biomed Imaging, 560 1St Ave, New York, NY 10016 USA
Babb, JS:
NYU, Dept Radiol, Sch Med, Ctr Biomed Imaging, 560 1St Ave, New York, NY 10016 USA
Blennow, K:
Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Psychiat, Dept Psychiat & Neurochem, Molndal, Sweden
Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden
Zetterberg, H:
Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Psychiat, Dept Psychiat & Neurochem, Molndal, Sweden
Sahlgrens Univ Hosp, Clin Neurochem Lab, Molndal, Sweden
UCL Inst Neurol, Dept Mol Neurosci, Queen Sq, London, England
Lu, SE:
Rutgers Sch Publ Hlth, Dept Biostat, Piscataway, NJ USA
Badia, SG:
Hosp Santa Creu & Sant Pau, Resp Dept, Sleep Unit, Barcelona, Spain
CIBERSAM, Inst Biomed Res St Pau, Barcelona, Spain
Univ Barcelona, Dept Clin Psychol & Psychobiol, Barcelona, Spain
Romero, S:
Univ Politecn Cataluna, Biomed Engn Res Ctr, Dept Automat Control, Barcelona, Spain
CIBER Bioingn Biomat & Nanomed, Barcelona, Spain
Rosenzweig, I:
Kings Coll London, Sleep & Brain Plast Ctr, Dept Neuroimaging, Inst Psychiat Psychol & Neurosci, London, England
GSTT NHS Trust, Guys & St Thomas Hosp, Sleep Disorders Ctr, London, England
Gosselin, N:
Hosp Sacre Coeur Montreal, Ctr Adv Res Sleep Med, Montreal, PQ, Canada
Univ Montreal, Dept Psychol, Montreal, PQ, Canada
Jean-Louis, G:
NYU, Ctr Healthful Behav Change, Langone Med Ctr, Div Hlth & Behav,Dept Populat Hlth, New York, NY USA
Rapoport, D:
Icahn Sch Med Mt Sinai, Div Pulm Crit Care & Sleep Med, New York, NY 10029 USA
de Leon, MJ:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Ayappa, I:
Icahn Sch Med Mt Sinai, Div Pulm Crit Care & Sleep Med, New York, NY 10029 USA
Osorio, RS:
NYU, Dept Psychiat, Langone Med Ctr, Ctr Brain Hlth, 550 1St Ave, New York, NY 10016 USA
Green Published
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