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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Adenosine Deaminase Polymorphism Affects Sleep EEG Spectral Power in a Large Epidemiological Sample

Texto completo
Autor(es):
Mazzotti, Diego Robles [1] ; Guindalini, Camila [1, 2] ; Lino de Souza, Altay Alves [1] ; Sato, Joao Ricardo [3] ; Santos-Silva, Rogerio [1] ; Azeredo Bittencourt, Lia Rita [1] ; Tufik, Sergio [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo, Dept Psicobiol, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Psiquiatria, Lab Neurociencias Clin LiNC, Sao Paulo - Brazil
[3] Univ Fed ABC, Ctr Matemat Comp & Cognicao, Santo Andre - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo Científico
Fonte: PLoS One; v. 7, n. 8 AUG 29 2012.
Citações Web of Science: 17
Resumo

Slow wave oscillations in the electroencephalogram (EEG) during sleep may reflect both sleep need and intensity, which are implied in homeostatic regulation. 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. 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 Sao Paulo, Brazil. Eight-hundred individuals were subjected to full-night polysomnography and ADA G22A genotyping. Spectral analysis of the EEG was carried out in all individuals using fast Fourier transformation of the signals from each EEG electrode. 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. 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. These changes were seen both in the whole sample and in the matched subset. The higher EEG spectral power indicates that the sleep of individuals carrying the A allele may be more intense. Therefore, this polymorphism may be an important source of variation in sleep homeostasis in humans, through modulation of specific components of the sleep EEG. (AU)

Processo FAPESP: 98/14303-3 - Center for Sleep Studies
Beneficiário:Sergio Tufik
Linha de fomento: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs