PMID- 18520330
OWN - NLM
STAT- MEDLINE
DCOM- 20080626
LR  - 20211020
IS  - 0031-3998 (Print)
IS  - 1530-0447 (Electronic)
IS  - 0031-3998 (Linking)
VI  - 63
IP  - 6
DP  - 2008 Jun
TI  - Diffuse axonal injury in periventricular leukomalacia as determined by apoptotic 
      marker fractin.
PG  - 656-61
LID - 10.1203/PDR.0b013e31816c825c [doi]
AB  - Periventricular leukomalacia (PVL), the major substrate of neurologic deficits in 
      premature infants, is associated with reduced white matter volume. Using 
      immunomarkers of axonal pathology [beta-amyloid precursor protein (beta-APP) and 
      apoptotic marker fractin], we tested the hypothesis that widespread (diffuse) 
      axonal injury occurs in the gliotic white matter beyond the foci of necrosis in 
      PVL, thus contributing to the white matter volume reduction. In a cohort of 17 
      control cases and 13 PVL cases with lesions of different chronological ages, 
      diffuse axonal damage in PVL was detected by fractin in white matter sites 
      surrounding and distant from acute and organizing foci of necrosis. Using 
      beta-APP, axonal spheroids were detected within necrotic foci in the acute and 
      organizing (subacute) stages, a finding consistent with others. Interestingly, 
      GAP-43 expression was also detected in spheroids in the necrotic foci, suggesting 
      attempts at axonal regeneration. Thirty-one percent of the PVL cases had thalamic 
      damage and 15% neuronal injury in the cerebral cortex overlying PVL. We conclude 
      that diffuse axonal injury, as determined by apoptotic marker fractin, occurs in 
      PVL and that its cause likely includes primary ischemia and trophic degeneration 
      secondary to corticothalamic neuronal damage.
FAU - Haynes, Robin L
AU  - Haynes RL
AD  - Department of Pathology, Children's Hospital and Harvard Medical School, Boston, 
      Massachusetts 02115, USA. robin.haynes@childrens.harvard.edu
FAU - Billiards, Saraid S
AU  - Billiards SS
FAU - Borenstein, Natalia S
AU  - Borenstein NS
FAU - Volpe, Joseph J
AU  - Volpe JJ
FAU - Kinney, Hannah C
AU  - Kinney HC
LA  - eng
GR  - P01 NS038475/NS/NINDS NIH HHS/United States
GR  - P01 NS038475-09/NS/NINDS NIH HHS/United States
GR  - P30-HD18655/HD/NICHD NIH HHS/United States
GR  - P30 HD018655/HD/NICHD NIH HHS/United States
GR  - P01-NS38475/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Actins)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (GAP-43 Protein)
SB  - IM
MH  - Actins/*analysis
MH  - Amyloid beta-Protein Precursor/analysis
MH  - *Apoptosis
MH  - Autopsy
MH  - Axons/chemistry/*pathology
MH  - Case-Control Studies
MH  - Cerebral Cortex/chemistry/pathology
MH  - Cerebrum/chemistry/*pathology
MH  - Diffuse Axonal Injury/*etiology/metabolism/pathology
MH  - GAP-43 Protein/analysis
MH  - Humans
MH  - Infant
MH  - Infant, Newborn
MH  - Leukomalacia, Periventricular/*complications/metabolism/pathology
MH  - Necrosis
MH  - Thalamus/chemistry/pathology
PMC - PMC2770332
MID - NIHMS112447
EDAT- 2008/06/04 09:00
MHDA- 2008/06/27 09:00
PMCR- 2009/10/29
CRDT- 2008/06/04 09:00
PHST- 2008/06/04 09:00 [pubmed]
PHST- 2008/06/27 09:00 [medline]
PHST- 2008/06/04 09:00 [entrez]
PHST- 2009/10/29 00:00 [pmc-release]
AID - 00006450-200806000-00012 [pii]
AID - 10.1203/PDR.0b013e31816c825c [doi]
PST - ppublish
SO  - Pediatr Res. 2008 Jun;63(6):656-61. doi: 10.1203/PDR.0b013e31816c825c.