PMID- 9329457
OWN - NLM
STAT- MEDLINE
DCOM- 19971031
LR  - 20190512
IS  - 0022-3069 (Print)
IS  - 0022-3069 (Linking)
VI  - 56
IP  - 10
DP  - 1997 Oct
TI  - Temporal and regional patterns of axonal damage following traumatic brain injury: 
      a beta-amyloid precursor protein immunocytochemical study in rats.
PG  - 1132-41
AB  - Diffuse axonal injury (DAI) is an important consequence of human head trauma. 
      This experimental investigation utilized the immunocytochemical visualization of 
      beta-amyloid precursor protein (beta-APP) to document regional patterns of axonal 
      injury after traumatic brain injury (TBI) and to determine the importance of 
      injury severity on the magnitude of axonal damage. Rats underwent moderate 
      (1.84-2.11 atm) or severe (2.38-2.52 atm) parasagittal fluid-percussion (F-P) 
      brain injury or sham procedures. At 1, 3, 7 or 30 days after TBI, rats were 
      perfusion-fixed and sections immunostained for the visualization of beta-APP. A 
      regionally specific axonal response to TBI was documented after moderate F-P 
      injury. Within the dorsolateral striatum, an early increase in beta-APP-positive 
      axonal profiles at 24 hours (h) was followed by a significant decline at 
      subsequent survival periods. In contrast, the frequency of reactive profiles was 
      initially low within the thalamus, but increased significantly by day 7. Within 
      the external capsule at the injury epicenter, numbers of immunoreactive axons 
      increased significantly at 24 h and remained elevated throughout the subsequent 
      survival periods. At multiple periods after TBI, selective cortical and thalamic 
      neurons displayed increased staining of the perikarya. A significant increase in 
      the overall frequency of beta-APP profiles was documented in the severe vs 
      moderately injured rats at 72 h after TBI. These data indicate that parasagittal 
      F-P brain injury (a) results in widespread axonal damage, (b) that axonal damage 
      includes both reversible and delayed patterns, and (c) that injury severity is an 
      important factor in determining the severity of the axonal response to TBI.
FAU - Bramlett, H M
AU  - Bramlett HM
AD  - Department of Neurology, University of Miami School of Medicine, FL 33101, USA.
FAU - Kraydieh, S
AU  - Kraydieh S
FAU - Green, E J
AU  - Green EJ
FAU - Dietrich, W D
AU  - Dietrich WD
LA  - eng
GR  - NS30291/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neuropathol Exp Neurol
JT  - Journal of neuropathology and experimental neurology
JID - 2985192R
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Biomarkers)
SB  - IM
MH  - Amyloid beta-Protein Precursor/*analysis/metabolism
MH  - Animals
MH  - Axons/metabolism/*pathology
MH  - Biomarkers
MH  - Brain/metabolism/*pathology
MH  - Brain Injuries/metabolism/*pathology/physiopathology
MH  - Corpus Striatum/pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Organ Specificity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Thalamus/pathology
MH  - Time Factors
EDAT- 1997/11/05 00:00
MHDA- 1997/11/05 00:01
CRDT- 1997/11/05 00:00
PHST- 1997/11/05 00:00 [pubmed]
PHST- 1997/11/05 00:01 [medline]
PHST- 1997/11/05 00:00 [entrez]
AID - 10.1097/00005072-199710000-00007 [doi]
PST - ppublish
SO  - J Neuropathol Exp Neurol. 1997 Oct;56(10):1132-41. doi: 
      10.1097/00005072-199710000-00007.