It has been found that this functional polymorphism leads to a decrease in ADA activity in erythrocytes and lymphocytes, thus being a candidate variant in the regulation of adenosine-dependent sleep homeostasis. Ī common functional variant of the ADA gene has been described as a G to A transition ( ADA G22A rs73598374) which leads to the substitution of asparagine for aspartic acid at the eightieth codon of the gene. Adenosine deaminase (ADA) is an enzyme that irreversibly metabolizes adenosine to inosine, and may therefore modify the need for slow wave sleep during extended wakefulness. The balance between adenosine production and degradation is controlled by an extensive network of enzymes, receptors, and transporters, which determines its intra- and extra-cellular concentration. This neuromodulator is increased in the basal forebrain during prolonged wakefulness, and is highly correlated with slow wave activity in NREM sleep, , supporting its role in homeostatic control. Īdenosine is a product of adenosine triphosphate metabolism, and is a signaling molecule described as a “sleep-promoting” substance. A growing body of evidence suggests the participation of several neuromodulators in the homeostatic control of the sleep-wake cycle, with the adenosinergic system playing a relevant role. Sleep is thought to be controlled by two processes: circadian and homeostatic regulation. Studies have shown that individual EEG profiles in non-rapid eye movement (NREM) and REM sleep are genetically determined, being one of the most heritable traits in humans identified so far,. The electroencephalogram (EEG) is a valuable tool for the characterization of brain wave oscillations seen across sleep stages. Sleep is a complex behavior that can be understood as an active process finely regulated and influenced by genetic and environmental factors. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: This study was supported by Associação Fundo de Incentivo à Psicofarmacologia (AFIP) and Fundação de Amparo à Pesquisa do Estado de São Paulo (CEPID #98/14303-3).
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Received: ApAccepted: JPublished: August 29, 2012Ĭopyright: © Mazzotti et al.
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(2012) Adenosine Deaminase Polymorphism Affects Sleep EEG Spectral Power in a Large Epidemiological Sample. Therefore, this polymorphism may be an important source of variation in sleep homeostasis in humans, through modulation of specific components of the sleep EEG.Ĭitation: Mazzotti DR, Guindalini C, de Souza AAL, Sato JR, Santos-Silva R, Bittencourt LRA, et al. The higher EEG spectral power indicates that the sleep of individuals carrying the A allele may be more intense. These changes were seen both in the whole sample and in the matched subset. When compared with homozygous GG genotype carriers, A allele carriers showed higher delta spectral power in Stage 1 and Stages 3+4 of sleep, and increased theta spectral power in Stages 1, 2 and REM sleep. The genotype groups were compared in the whole sample and in a subsample of 120 individuals matched according to ADA genotype for age, gender, body mass index, caffeine intake status, presence of sleep disturbance, and sleep-disturbing medication. Spectral analysis of the EEG was carried out in all individuals using fast Fourier transformation of the signals from each EEG electrode.
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Eight-hundred individuals were subjected to full-night polysomnography and ADA G22A genotyping. The present study verified the association between the ADA G22A polymorphism and changes in sleep EEG spectral power (from C3-A2, C4-A1, O1-A2, and O2-A1 derivations) in the Epidemiologic Sleep Study (EPISONO) sample from São Paulo, Brazil. Adenosine is strongly implicated in sleep homeostasis, and a single nucleotide polymorphism in the adenosine deaminase gene ( ADA G22A) has been associated with deeper and more efficient sleep. Slow wave oscillations in the electroencephalogram (EEG) during sleep may reflect both sleep need and intensity, which are implied in homeostatic regulation.