Neuronal apoptosis in sudden infant death syndrome

Citation
Ka. Waters et al., Neuronal apoptosis in sudden infant death syndrome, PEDIAT RES, 45(2), 1999, pp. 166-172
Citations number
52
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
PEDIATRIC RESEARCH
ISSN journal
00313998 → ACNP
Volume
45
Issue
2
Year of publication
1999
Pages
166 - 172
Database
ISI
SICI code
0031-3998(199902)45:2<166:NAISID>2.0.ZU;2-D
Abstract
Although evidence shows that victims of sudden infant death syndrome (SIDS) suffer repetitive episodes of hypoxemia, only subtle abnormalities have be en found in their brains by Light microscopy. The aim of the present study was to determine whether apoptosis, a form of cell death that can be trigge red by hypoxemia and that leaves no scarring detectable by light microscopy , would be present in hypoxia-sensitive brain regions of SIDS victims. We l ooked for the presence of apoptosis with an in situ end-labeling method tha t detects DNA fragmentation. We studied 29 SIDS victims who were age-matche d to nine control cases. We found significant neuronal apoptosis in 79% of the SIDS cases: 55% of the cases positive in the hippocampus and 96% positi ve in the brainstem. Whereas the distribution of apoptosis in the hippocamp us was in hypoxia-sensitive subregions, the distribution in the brainstem w as mostly in dorsal nuclei, including those involved with sensation in the face and position of the head (nucleus of the spinal trigeminal tract and v estibular nuclei). The control cases showed no significant apoptosis in the hippocampus and a mild degree in the brainstem in three cases. Our results indicate the occurrence of an acute insult at least several hours before d eath, an insult from which the infants had apparently recuperated. This sug gests that SIDS victims suffered repeated apoptosis resulting in significan t neuronal damage and, thus, functional loss in key brain regions. The invo lvement of specific nuclei in the brainstem may be Linked to the fact that prone sleeping is a significant risk factor for SIDS. Enhanced neuronal dea th by apoptosis may thus have major implications for understanding the sequ ence of events leading to SIDS.