PMID- 15749363
OWN - NLM
STAT- MEDLINE
DCOM- 20050526
LR  - 20061115
IS  - 0379-0738 (Print)
IS  - 0379-0738 (Linking)
VI  - 149
IP  - 2-3
DP  - 2005 May 10
TI  - Apnea, glial apoptosis and neuronal plasticity in the arousal pathway of victims 
      of SIDS.
PG  - 205-17
AB  - Of 27,000 infants whose sleep-wake characteristics were studied under the age of 
      6 months, 38 died unexpectedly 2-12 weeks after the sleep recording in a 
      pediatric sleep laboratory. Of these infants, 26 died of sudden infant death 
      syndrome (SIDS), and 12 of definitely identified causes. The frequency and 
      duration of sleep apneas were analysed. Sleep recordings and brainstem 
      histopathology were studied to elucidate the possible relationship between sleep 
      apnea and neuropathological changes within the arousal system. 
      Immunohistochemical analyses were conducted using tryptophan hydroxylase (TrypH), 
      a serotonin synthesizing enzyme, and growth-associated phosphoprotein 43 (GAP43), 
      a marker of synaptic plasticity. The terminal-deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) method was used for 
      apoptosis. The pathological and physiological data were correlated for each 
      infant. In the SIDS victims, statistically significant positive correlations were 
      seen between the number of TrypH-positive neurons in the dorsal raphe nucleus of 
      the midbrain and the duration of central apneas (p = 0.03), between the number of 
      TUNEL-positive glial cells in the pedunculopontine tegmental nucleus (PPTN) and 
      the average number of spines in GAP43-positive neurons in the PPTN (p = 0.04). 
      These findings in the dorsal raphe nucleus of the midbrain and PPTN, that play 
      important roles in the arousal pathway suggest a possible link between changes in 
      arousal and SIDS.
FAU - Sawaguchi, T
AU  - Sawaguchi T
AD  - Department of Legal Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, 
      Shinjuku, 162-8666 Tokyo, Japan. tsawagu@research.ywmu.ac.jp
FAU - Kato, I
AU  - Kato I
FAU - Franco, P
AU  - Franco P
FAU - Sottiaux, M
AU  - Sottiaux M
FAU - Kadhim, H
AU  - Kadhim H
FAU - Shimizu, S
AU  - Shimizu S
FAU - Groswasser, J
AU  - Groswasser J
FAU - Togari, H
AU  - Togari H
FAU - Kobayashi, M
AU  - Kobayashi M
FAU - Nishida, H
AU  - Nishida H
FAU - Sawaguchi, A
AU  - Sawaguchi A
FAU - Kahn, A
AU  - Kahn A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Forensic Sci Int
JT  - Forensic science international
JID - 7902034
RN  - 0 (GAP-43 Protein)
RN  - EC 1.14.16.4 (Tryptophan Hydroxylase)
SB  - IM
MH  - *Apoptosis
MH  - Case-Control Studies
MH  - Female
MH  - Forensic Medicine
MH  - GAP-43 Protein/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Infant
MH  - Infant, Newborn
MH  - Male
MH  - Neuroglia/*metabolism
MH  - Neurons/metabolism
MH  - Pedunculopontine Tegmental Nucleus/metabolism
MH  - Polysomnography
MH  - Raphe Nuclei/metabolism
MH  - Sleep Apnea, Central/*metabolism
MH  - Sudden Infant Death/*pathology
MH  - Tryptophan Hydroxylase/metabolism
EDAT- 2005/03/08 09:00
MHDA- 2005/05/27 09:00
CRDT- 2005/03/08 09:00
PHST- 2005/03/08 09:00 [pubmed]
PHST- 2005/05/27 09:00 [medline]
PHST- 2005/03/08 09:00 [entrez]
AID - S0379-0738(04)00687-5 [pii]
AID - 10.1016/j.forsciint.2004.10.015 [doi]
PST - ppublish
SO  - Forensic Sci Int. 2005 May 10;149(2-3):205-17. doi: 
      10.1016/j.forsciint.2004.10.015.