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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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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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“Many biological pathways are disrupted by experimental TBI resulting in progressive neurodegeneration including atrophy, neuronal loss, and axonal degeneration which are often associated with neuroinflammation including macrophage reactivity (82–85).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [85]
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“Given behavioral deficits in pre-clinical models have been observed up to 1 year after experimental injury [40, 41], identifying underlying molecular changes in the subacute to chronic phases of TBI are key to understanding potential rehabilitation strategies.”
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“…progressive brain atrophy and ventricle enlargement (Bergeson et al., 2004; Bigler and Maxwell, 2011), while imaging of animal models of TBI demonstrates progressive increase in the volume of the cavity under the impact site (Bramlett and Dietrich, 2002; Dixon et al., 1999; Pierce et al., 1998).”
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Cortical-wide impairment of “The Glymphatic system” after focal brain injuryPreprint
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“…of cerebral circulation seen 1 week after light injury likely increases the risk of memory impairment, depression, and epilepsy, which are known to be related to brain injury, due to the accumulation of waste products and ionic environmental imbalances (Pierce et al., 1998; Salazar et al., 1985).”
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Struggling with Imperfect Instruments: A Brief History of Experimental Traumatic Brain Injury
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What Happens to Concussed Animals?
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Novel Genetic Models to Study the Role of Inflammation in Brain Injury-Induced Alzheimer's Pathology
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“Lateral FPI results in progressive cortical damage that continues beyond 6 months after injury (Pierce et al. 1998).”
BackgroundButler, C. R. (2016) · UKnowledge (University of Kentucky) · doi:10.13023/etd.2016.182
“This is one of the most well characterized brain injury models and demonstrates many of the hallmark features of TBI in human patients such as neuron loss, diffuse axonal injury, and cognitive impairment (Cortez et al., 1989;Lowenstein et al., 1992;Hicks et al., 1993;Rink et al., 1995;Bramlett et al., 1997;Hicks et al…”
BackgroundBiology of Neuroinflammation: A Common Denominator in Brain Pathologies
Tandon, P. (2016) · Springer eBooks · doi:10.1007/978-981-10-1711-7_1 · Cited by 1
Assessments of Cognitive Function Following Traumatic Brain Injury
Reid, W., & Sun, D. (2012) · doi:10.1007/978-1-61779-576-3_14
Nakagawa (1999) · doi:10.1002/(sici)1096-9861(19990830)411:3
Self-citationA unifying hypothesis of alzheimer’s disease: III—Risk factors
Heininger, K. (2000) · Human Psychopharmacology: Clinical and Experimental · doi:10.1002/(sici)1099-1077(200001)15:1
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
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 1998-07
- Volume
- 87
- Issue
- 2
- Pages
- 359-369
- ISSN
- 0306-4522 (ISSN-L)
- 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
- hybrid
- doi.org
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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