Interaction between sleep-disordered breathing and apolipoprotein E genotype on cerebrospinal fluid biomarkers for Alzheimer's disease in cognitively normal elderly individuals.

Publication Type Academic Article
Authors Osorio R, Ayappa I, Mantua J, Gumb T, Varga A, Mooney A, Burschtin O, Taxin Z, During E, Spector N, Biagioni M, Pirraglia E, Lau H, Zetterberg H, Blennow K, Lu S, Mosconi L, Glodzik L, Rapoport D, de Leon M
Journal Neurobiol Aging
Volume 35
Issue 6
Pagination 1318-24
Date Published 12/27/2013
ISSN 1558-1497
Keywords Alzheimer Disease, Amyloid beta-Peptides, Apolipoprotein E4, Genotype, Peptide Fragments, Respiration, Sleep Wake Disorders, tau Proteins
Abstract Previous studies have suggested a link between sleep disordered breathing (SDB) and dementia risk. In the present study, we analyzed the relationship between SDB severity, cerebrospinal fluid (CSF) Alzheimer's disease-biomarkers, and the ApoE alleles. A total of 95 cognitively normal elderly participants were analyzed for SDB severity, CSF measures of phosphorylated-tau (p-tau), total-tau (t-tau), and amyloid beta 42 (Aβ-42), as well as ApoE allele status. In ApoE3+ subjects, significant differences were found between sleep groups for p-tau (F[df2] = 4.3, p = 0.017), and t-tau (F[df2] = 3.3, p = 0.043). Additionally, among ApoE3+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was positively correlated with p-tau (r = 0.30, p = 0.023), t-tau (r = 0.31, p = 0.021), and Aβ-42 (r = 0.31, p = 0.021). In ApoE2+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was correlated with lower levels of CSF Aβ-42 (r = -0.71, p = 0.004), similarly to ApoE4+ subjects where there was also a trend toward lower CSF Aβ-42 levels. Our observations suggest that there is an association between SDB and CSF Alzheimer's disease-biomarkers in cognitively normal elderly individuals. Existing therapies for SDB such as continuous positive airway pressure could delay the onset to mild cognitive impairment or dementia in normal elderly individuals.
DOI 10.1016/j.neurobiolaging.2013.12.030
PubMed ID 24439479
PubMed Central ID PMC4022140
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