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The presence of TATA-binding protein in the brainstem, correlated with sleep apnea in SIDS victims

par Sawaguchi, Toshiko;Patricia, Franco;Kadhim, Hazim ;Groswasser, José ;Sottiaux, Martine;Nishida, Hiroshi;Kahn, André
Référence Early human development, 75, SUPPL. 1, page (S109-S118)
Publication Publié, 2003-12

Article révisé par les pairs

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Résumé :

Background: Recent reports have indicated that the presence of transcription factors and RNA polymerase decreases in rat brains that suffer perinatal asphyxia from hypoxia. As hypoxia has been proposed as a causative factor in the Sudden Infant Death Syndrome (SIDS), the correlation between TATA-binding protein (TBP) in the brainstem of SIDS victims as a marker of transcription and the incidence of sleep apnea was investigated. Materials and methods: A total of 38 infants, including 26 cases of SIDS, died under 6 months of age, in a cohort of 27,000 infants studied prospectively to characterize their sleep-wake behavior. The frequency and duration of sleep apnea was analyzed. Brainstem material was collected and immunohistochemistry of TBP was carried out. The density of TBP-positive neurons was measured quantitatively. Correlation analyses were carried out between the density of TBP-positive neurons and the data concerning sleep apnea. Results: One SIDS-specific positive correlation occurred between the density of TBP-positive neurons in the dorsal raphe nucleus of the midbrain and the duration of central apnea (p=0.049) and two SIDS-specific negative correlations between the density of TBP-positive neurons in the pars compacta and dissipata of the pedunculopontine tegmentum nucleus (PPTNc, PPTNd) in the midbrain and the duration of apnea (p=0.035). Conclusions: The significant correlation between the findings of TBP-positive neurons in the midbrain arousal pathway and the characteristics of sleep apnea in SIDS victims is in agreement with the both association of apnea and arousal phenomenon in pathophysiology of SIDS. © 2003 Elsevier Ireland Ltd. All rights reserved.