Temporal and regional patterns of axonal damage following traumatic brain injury: a beta-amyloid precursor protein immunocytochemical study in rats
Abstract
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 b…
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APP expression increases in striatal and hippocampal axons along with cortical and thalamic neurons within the first 24 h after experimental impact and fluid percussion TBI.
“For example, APP expression increases in striatal and hippocampal axons along with cortical and thalamic neurons within the first 24 h after experimental impact and fluid percussion TBI (121–123)”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [122]
A majority of rodent studies fail to show Aβ deposition after TBI in non-transgenic animals using CCI, FPI, and weight drop models.
“a majority of rodent studies fail to show this association in non-transgenic animals using CCI, FPI, and weight drop models (121, 122, 124, 125, 135).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [122]
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- Authors
- BRAMLETT, H. M., KRAYDIEH, S., GREEN, E. J., & DIETRICH, W. D.
- Affiliations
- University of Miami (US)
- Corresponding author
- DIETRICH, W. DALTON
- Venue
- Journal of Neuropathology and Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-10
- Volume
- 56
- Issue
- 10
- Pages
- 1132-1141
- ISSN
- 0022-3069 (ISSN-L)
- OpenAlex
- W2068493439
- Cited by
- 225
- References
- 0
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 5 · 2022: 5 · 2021: 2 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 6 · 2014: 11 · 2013: 10 · 2012: 10
- FWCI
- 7.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS-30291, P50NS030291)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Automotive and Human Injury Biomechanics
- Keywords
- traumatic brain injury, diffuse axonal injury, axonal injury, amyloid precursor protein, fluid percussion injury, injury severity, dorsolateral striatum, thalamus, external capsule, cortical neurons, perikarya
- MeSH terms
- Animals, Axons, Brain, Brain Injuries, Corpus Striatum, Humans, Immunohistochemistry, Male, Organ Specificity, Thalamus, Time Factors, Biomarkers, Amyloid beta-Protein Precursor, Rats, Sprague-Dawley, Rats
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