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Cited by 385Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchAutomotive and Human Injury Biomechanics

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Enduring cognitive, neurobehavioral and histopathological changes persist for up to one year following severe experimental brain injury in rats

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Pierce, J.E.S, Smith, D.H, Trojanowski, J.Q, McIntosh, T.K·1998·Neuroscience
DOI 10.1016/s0306-4522(98)00142-0
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Abstract

Clinical studies have demonstrated that patients sustain prolonged behavioral deficits following traumatic brain injury, in some cases culminating in the cognitive and histopathological hallmarks of Alzheimer's disease. However, few studies have examined the long-term consequences of experimental traumatic brain injury. In the present study, anesthetized male Sprague-Dawley rats (n = 185) were subjected to severe lateral fluid-percussion brain injury (n = 115) or sham injury (n = 70) and evaluated up to one year post-injury for cognitive and neurological deficits and histopathological changes. Compared with sham-injured controls, brain-injured animals showed a spatial learning impairment that persisted up to one year post-injury. In addition, deficits in specific neurologic motor function tasks also persisted up to one year post-injury. Immunohistochemistry using multiple antibodies to the amyloid precursor protein and/or amyloid precursor protein-like proteins revealed novel axonal degeneration in the striatum, corpus callosum and injured cortex up to one year post-injury and in the thalamus up to six months post-injury. Histologic evaluation of injured brains demonstrated a progressive expansion of the cortical cavity, enlargement of the lateral ventricles, deformation of the hippocampus, and thalamic calcifications. Taken together, these findings indicate that experimental traumatic brain injury can cause long-term cognitive and neurologic motor dysfunction accompanied by continuing neurodegeneration.

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Metadata

Authors
Pierce, J. E. S., Smith, D. H., Trojanowski, J. Q., & McIntosh, T. K.
Affiliations
  • UConn Health (US)
  • University of Pennsylvania (US)
Corresponding author
Smith, D.H
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
1998-07
Volume
87
Issue
2
Pages
359-369
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/s0306-4522(98)00142-0
OpenAlex
W2019544787
Cited by
385
References
61
Citations by year
2026: 2 · 2025: 8 · 2024: 9 · 2023: 10 · 2022: 10 · 2021: 11 · 2020: 16 · 2019: 16 · 2018: 16 · 2017: 11 · 2016: 21 · 2015: 15 · 2014: 15 · 2013: 22 · 2012: 14
FWCI
11.56
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuroscience (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG12527, R01AG012527)
  • National Institute of Neurological Disorders and Stroke (NS-08803, NS26818)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
  • Physical Sciences › Engineering › Biomedical Engineering › Automotive and Human Injury Biomechanics
Keywords
traumatic brain injury, fluid percussion injury, long-term cognitive deficits, spatial learning impairment, motor impairment, axonal degeneration, amyloid precursor protein, neurodegeneration, thalamic calcification, ventriculomegaly, Alzheimer's disease
MeSH terms
Animals, Behavior, Animal, Brain, Brain Chemistry, Brain Injuries, Cognition Disorders, Forelimb, Male, Psychomotor Performance, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Rats, Sprague-Dawley, Maze Learning, Rats

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