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Background: Recently, the appearance of beta-amyloid precursor protein (APP) has been demonstrated in the neonatal brain following hypoxic–ischaemic injury. As chronic hypoxia is one of the favoured theories of causation in the sudden infant death syndrome (SIDS), the correlation between APP in the brainstem and sleep apnea in SIDS was investigated. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, which included 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory, some 3 to 12 weeks before death. The frequency and duration of sleep apnea were analyzed. The brainstem material was collected and immunohistochemistry with anti-Alzheimer precursor protein A4 (APP) was carried out. The density of APP-positive elements was measured semi-quantitatively. Correlation analyses were carried out between the density of APP-positive elements and the data on sleep apnea. Results: No correlation was found. Conclusion: No correlation between pathological data of APP and physiological data of sleep apnea was not in agreement with the association of sleep apnea in pathophysiology of SIDS. [Copyright &y& Elsevier]

Background: In the Sudden Infant Death Syndrome (SIDS), a medullary serotonergic network deficiency theory has been proposed, amongst many other hypotheses. The correlation between serotonergic neurons or dendritic spines in the brainstem of SIDS and sleep apnea was investigated here. Materials and methods: Twenty-seven thousand infants were studied prospectively to characterize their sleep–wake behavior. Of these, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry for tryptophan hydroxylase (TrypH) carried out. The density of TrypH-positive neurons was measured quantitatively. Correlation analyses were carried out between the TrypH-associated pathological data and the physiological data of sleep apnea. Results: One significant positive correlation between the density of TrypH-positive neurons in the dorsal raphe nucleus of the midbrain and the duration of central apnea (p=0.027) was found in SIDS victims. Conclusions: Some of serotonergic facts could be involved in the pathophysiology of SIDS. [Copyright &y& Elsevier]

The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its cause is still unknown. A chronic hypoxic situation has been shown to exist in the brains of SIDS victims and apoptosis has been demonstrated in hypoxic situations. In this study, the correlation between apoptotic neurons or glias and sleep apnea in SIDS was investigated in the brainstem of SIDS victims. Materials and methods: In a cohort of 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. The brainstem material was collected and terminal-deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method was carried out. The density of TUNEL-positive neurons or glias was measured quantitatively. Correlation analyses were carried out between the apoptosis-associated pathological data and the physiological data of sleep apnea. Results: No significant negative or positive correlation between the density of TUNEL-positive neurons or glias and the characteristics of sleep apnea was observed in SIDS victims. No statistically significant differences associated with apoptotic neurons and glias were observed between SIDS and non-SIDS. Conclusions: The pathological findings of apoptosis were not in agreement with the hypothesis refer to apnea and arousal phenomenon in pathophysiology of SIDS. [Copyright &y& Elsevier]

Background: Chronic hypoxia, leading to brainstem gliosis, has been postulated as a factor in the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. Gliosis detected by immunohistochemistry of glial fibrillary acidic protein (GFAP) is a marker of apoptosis. The correlation between GFAP-positive reactive astrocytes in the brainstem and sleep apnea in SIDS was investigated. Materials and Methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry of GFAP carried out. The density of GFAP-positive reactive astrocytes was measured quantitatively. Correlation analyses were carried out between the data on gliosis and the physiological data of sleep apnea. Results: A SIDS-specific negative correlation between the density of gliosis in the dorsal vagus nucleus in the medulla oblongata and the frequency of obstructive apnea (p=0.022) was found. Conclusions: A significant SIDS-specific correlation with gliosis in the dorsal vagus nucleus and the characteristics of sleep apnea might invite the cardiorespiratory changes in SIDS. [Copyright &y& Elsevier]

Background: The Ki-67 antigen appears in all human proliferating cells during late G1, S, M and G2 phases of the cell cycle, but is consistently absent in the Go phase (noncycling) cells. The correlation between Ki-67 in the brainstem and sleep apnea in victims of the sudden infant death syndrome (SIDS) was investigated to elucidate cell kinetics in the brainstem of this condition, which is still the main cause of postneonatal infant death. Materials and Methods: Twenty-six cases of SIDS occurred among 38 infants dying under 6 months of age in a cohort of 27,000 infants studied prospectively to characterize their sleep–wake behavior. All the infants had been recorded during one night in a pediatric sleep laboratory some 3 to 12 weeks before death. The frequency and duration of sleep apnea were analyzed. At autopsy, brainstem material was collected and immunohistochemistry for Ki-67 was carried out. The density of Ki-67-positive neurons was measured semiquantitatively. Correlation analyses were carried out between the density of Ki-67-positive neurons and the data on sleep apnea. Results: Except in two cases in SIDS victims and in one control, the detection of Ki-67 was negative. No correlation analysis between the Ki-67 and of sleep apnea was found. Conclusions: There were no abnormal cell kinetics detected by the demonstration of Ki-67 antigen in the brainstems of SIDS victims. [Copyright &y& Elsevier]

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. [Copyright &y& Elsevier]

Background: Recently, it has been reported that neuronal plasticity in the brainstem arousal pathway is related to the sudden infant death syndrome (SIDS). Tau protein may contribute to axonal development and neural plasticity; therefore, the correlation between τ protein in the brainstem and sleep apnea in SIDS was investigated here. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed on all the infants, having been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The brainstem material was collected and immunohistochemistry of τ was carried out. The density of τ-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of τ-positive elements and the data of sleep apnea. Results: In the 26 SIDS cases, τ-positive findings were observed in the sub-pia mater in two cases, in the colloid plexus in one case, in the ependyma and subependyma in five cases, in neurons in two cases and as a general diffusion in one case. In 12 control cases, τ-positive findings were observed in the sub-pia mater in one case and in neuronal elements in three cases. No correlation was found on analysis. Conclusions: There was no correlation between the finding of τ in the brainstem of SIDS victims and the incidence of sleep apnea. [Copyright &y& Elsevier]

Background: Microtubule-associated protein 2(MAP2), a cytoskeletal protein of the neuron, is a marker of early ischemic neuronal damage. As a chronic hypoxic situation exists in the brains of victims of the sudden infant death syndrome (SIDS), the correlation between MAP2-positive neurons or dendritic spines in the brainstem and sleep apnea was investigated in SIDS, which is still the main cause of postneonatal infant death. Materials and methods: 27,000 infants were studied prospectively to characterize their sleep–wake behavior and amongst these, 38 infants died under 6 months of age. They included 26 cases of SIDS. The frequency and duration of sleep apneae were analyzed. The brainstem material was collected and immunohistochemistry of MAP2 was carried out. The density of MAP2-positive neurons, dendrites and dendritic spines were measured quantitatively. Correlation analyses were carried out between the MAP2-associated pathological data and the physiological data of sleep apnea. Results: One negative correlation between the density of MAP2-positive dendrites in the pars compacta of pedunculo-pontine tegmentum nucleus (PPTNc) and the duration of obstructive apnea (p=0.017) and two SIDS-specific positive correlations between the density of MAP2-positive dendrites in the pars dissipata of pedunculo-pontine tegmentum nucleus (PPTNd) and the duration of central apnea (p=0.005) and between the dorsal raphe and the frequency of obstructive apnea were found in SIDS victims. The density of MAP2-positive dendritic spines in PPTNc was significantly higher in SIDS than in control (p=0.034). Conclusions: The significant correlations with the MAP2-positive findings in the midbrain arousal pathway and the characteristics of sleep apnea in SIDS victims were in agreement with the association with apnea and arousal-deficiency in SIDS. [Copyright &y& Elsevier]

Background: The sudden infant death syndrome (SIDS) is still the main cause of postneonatal infant death and its etiology has stimulated many competing theories, among which is the role of hypoxia and brainstem abnormalities. One report claims an increased in ubiquitin in the liver of SIDS victims, ubiquitin being one of the heat-shock proteins. The correlation between ubiquitin in the brainstem and sleep apnea in SIDS was investigated here. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected at autopsy and examined immunohistochemically for ubiquitin. The density of ubiquitin-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of ubiquitin-positive elements and the data on sleep apnea. Results: In the victims of SIDS, a statistically significant positive correlation was found between the density of ubiquitin-positive neuronal factors in the pons and the frequency of obstructive apnea (p=0.001) and statistically significant negative correlations were seen between the density of ubiquitin-positive cells in the ependyma in the pons and the duration of obstructive apnea (p=0.044) and between the density of ubiquitin-positive cells in the subependyma in the medulla and the frequency of central apnea (p=0.024). Conclusions: It was found that three significant associations existed between the pathological data referring to ubiquitin and physiological data in SIDS victims. These facts are in agreements with the association of sleep apnea in SIDS. [Copyright &y& Elsevier]

Background: Recently it has been reported that serotonin and related matters are associated with the sudden infant death syndrome (SIDS), which is still the main cause of postneonatal infant death. To further explore this claim, the correlation between serotonin receptors in the brainstem and sleep apnea in SIDS victims was investigated. Materials and methods: Among 27,000 infants studied prospectively to characterize their sleep–wake behavior, 38 infants died under 6 months of age including 26 cases of SIDS. All the infants had been recorded during one night in a pediatric sleep laboratory some 3–12 weeks before death. The frequency and duration of sleep apnea were analyzed. Brainstem material was collected and immunohistochemistry on 5-hydroxy tryptamine 1A (5HT1A) receptor was carried out. The density of 5HT1A receptor-positive neurons was measured quantitatively. Nonparametric analysis of the density of 5HT1A receptor-positive neurons was carried out between SIDS and non-SIDS cases. Correlation analyses were performed between the density of 5HT1A receptor-positive neurons and the data on sleep apnea. Results: There was no correlation between the pathological data on 5HT1A receptors and the physiological data on sleep apnea in SIDS victims. Conclusions: No correlation between pathological findings of serotonin and physiological findings of sleep apnea were not in agreement with the association of sleep apnea in pathophysiology of SIDS. [Copyright &y& Elsevier]