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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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Rao, V. L. R., Dogan, A., Bowen, K., & Dempsey, R. (2000) · Experimental Neurology · doi:10.1006/exnr.1999.7269 · Cited by 183
Prolonged Activation of NF-κB Following Traumatic Brain Injury in Rats
NONAKA, M., CHEN, X.-H., PIERCE, J. E. S., LEONI, M. J., McINTOSH, T. K., WOLF, J. A., & SMITH, D. H. (1999) · Journal of Neurotrauma · doi:10.1089/neu.1999.16.1023 · Cited by 176
Self-citationHallam, T. M., Floyd, C. L., Folkerts, M. M., Lee, L. L., Gong, Q.-Z., Lyeth, B. G., Muizelaar, J. P., & Berman, R. F. (2004) · Journal of Neurotrauma · doi:10.1089/089771504774129865 · Cited by 162
“…produced by both injury methods are consistent with the previous reports demonstrating significant motor deficits following LFP (Hamm et al., 1994; Pierce et al., 1998; Hamm, 2001) and WDIA (Beaumont et al., 1999; Heath et al., 1999; Berman et al., 2000; Schmidt et al., 2000; Maughan et al.,…”
Traumatic axonal injury: practical issues for diagnosis in medicolegal cases
Geddes, J., Whitwell, H., & Graham, D. I. (2000) · Neuropathology and Applied Neurobiology · doi:10.1046/j.1365-2990.2000.026002105.x · Cited by 169
Repeated Mild Traumatic Brain Injury
Fehily, B., & Fitzgerald, M. (2017) · Cell Transplantation · doi:10.1177/0963689717714092 · Cited by 240
“In contrast, ionic restoration can lead to axonal recovery,(204) while a host of secondary injury mechanisms likely contribute to progressive axonal degeneration.(200,205) Hyperphosphorylation of tau also occurs in TBI,(206) resulting in reduced microtubule binding,(207) which causes disassembly of microtubules and th…”
BackgroundSynaptogenesis in the Hippocampal CA1 Field following Traumatic Brain Injury
Scheff, S., Price, D., Hicks, R., Baldwin, S. A., Robinson, S., & Brackney, C. (2005) · Journal of Neurotrauma · doi:10.1089/neu.2005.22.719 · Cited by 167
“TBI-related cognitive deficits related to spatial learning can persist as long as 1 year post-injury in these animal models (Pierce et al., 1998; Dixon et al., 1999), whereas significant motor skills deficits are more transient.”
Kline, A. E., Massucci, J. L., Marion, D. W., & Dixon, C. E. (2002) · Journal of Neurotrauma · doi:10.1089/08977150252932370 · Cited by 147
“…produce spatial learning acquisition deficits in adult rats (Smith et al., 1991; Hoff-man et al., 1994; Bramlett et al., 1997; Scheff et al., 1997; Pierce et al., 1998; Dixon et al., 1999a,b; Sanders et al., 1999; Kline et al., 2000), immature rats (Prins and Hovda, 1998; Adelson et al., 2000),…”
Fluid-percussion–induced traumatic brain injury model in rats
Kabadi, S. V., Hilton, G. D., Stoica, B. A., Zapple, D. N., & Faden, A. I. (2010) · Nature Protocols · doi:10.1038/nprot.2010.112 · Cited by 170
“This test is extremely reliable for evaluating TBI-induced motor impairment from hours to 1 year after FP injur”
Applications of the Morris water maze in translational traumatic brain injury research
Tucker, L. B., Velosky, A. G., & McCabe, J. T. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.03.010 · Cited by 163
“…for at least one year after the injury (Abrahamson et al., 2009; Dixon et al., 1999; Lindner et al., 1998; Mannix et al., 2013; Meehan et al., 2012; Pierce et al., 1998; Sell et al., 2017; Shear et al., 2004), providing an excellent context in which the effects of treatments on long-term recovery…”
Smith, D. C., Modglin, A., Roosevelt, R. W., Neese, S., Jensen, R. A., Browning, R., & Clough, R. (2005) · Journal of Neurotrauma · doi:10.1089/neu.2005.22.1485 · Cited by 141
Self-citationSpain, A., Daumas, S., Lifshitz, J., Rhodes, J. K. J., Andrews, P., Horsburgh, K. J., & Fowler, J. H. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2010.1288 · Cited by 139
“Moststudies have focused on moderate to severe levels of injury, which produce gross damage to grey and white matter regions, particularly the hippocampus (Carbonell et al., 1998; Holland et al., 2008; Pierce et al., 1998, 1996; Tran et al., 2006; Witgen et al., 2005).”
Webster, K. M., Wright, D. K., Sun, M., Semple, B. D., Öztürk, E., Stein, D. G., O'Brien, T. J., & Shultz, S. R. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0457-7 · Cited by 137
“Of particular note, the sensorimotor cortex is situated near the FPI impact area [27, 56, 57], and damage to the cortex and hippocampus has been linked to cognitive and sensorimotor deficits in TBI [27, 58 – 61].”
BackgroundThalamic Nuclei After Human Blunt Head Injury
Maxwell, W., MacKinnon, M., Smith, D. H., McIntosh, T., & Graham, D. (2006) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/01.jnen.0000229241.28619.75 · Cited by 132
“After traumatic brain injury (TBI), there is impairment of cognitive and memory functions in both humans (5) and experimental animals (6, 7).”
BackgroundSelf-citationOsteen, C. L., Moore, A. H., Prins, M., & Hovda, D. (2001) · Journal of Neurotrauma · doi:10.1089/08977150150502587 · Cited by 131
“…1990; Shirotani et al., 1994; Watanabe et al., 2000a,b; Stein and Vannucci, 1988; Soares et al., 1995; Smith et al., 1997; Bramlett et al., 2000; Pierce et al., 1998; Kolb et al., 1983, 1986), selective neuronal death of thalamic nuclei is thought to be due to retrograde degeneration resulting…”
Environmental enrichment and the sensory brain: The role of enrichment in remediating brain injury
Alwis, D. S., & Rajan, R. (2014) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2014.00156 · Cited by 129
“This is not a simple endeavor since neurodegeneration caused by TBI occurs as a result of a number of complex and dynamic inter-related mechanisms (Smith et al., 1991; Hicks et al., 1993; Pierce et al., 1998; Hall and Lifshitz, 2010; McNamara et al., 2010).”
BackgroundThe Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease
Kokiko-Cochran, O. N., & Godbout, J. P. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00672 · Cited by 128
Pullela, R., Raber, J., Pfankuch, T., Ferriero, D. M., Claus, C. P., Koh, S., Yamauchi, T., Rola, R., Fike, J. R., & Noble‐Haeusslein, L. J. (2006) · Developmental Neuroscience · doi:10.1159/000094166 · Cited by 134
Begum, G., Yan, H. Q., Li, L., Singh, A., Dixon, C. E., & Sun, D. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.2872-13.2014 · Cited by 130
“Axonal pathology has been shown to develop over the course of hours to days following injury and has even been observed for months (Christman et al., 1994; Pierce et al., 1998).”
BackgroundWilde, E., Bigler, E. D., Hunter, J. V., Fearing, M. A., Scheibel, R., Newsome, M., Johnson, J. L., Bachevalier, J., Li, X.-Q., & Levin, H. S. (2007) · Developmental Medicine & Child Neurology · doi:10.1111/j.1469-8749.2007.00294.x · Cited by 125
The lesion(s) in traumatic brain injury: implications for clinical neuropsychology
Bigler, E. D. (2001) · Archives of Clinical Neuropsychology · doi:10.1016/s0887-6177(00)00095-0 · Cited by 256
Hutson, C. B., Lazo, C. R., Mortazavi, F., Giza, C. C., Hovda, D. A., & Chesselet, M. (2011) · Journal of Neurotrauma · doi:10.1089/neu.2010.1723 · Cited by 133
“One of the attributes of the LFP model of TBI is its ability to model axonal injury (Graham et al., 2000; Pierce et al., 1998), a common consequence of TBI (Maxwell et al., 1997).”
BackgroundInfluentialExperimental models of brain trauma
Laurer, H. L., & McIntosh, T. K. (1999) · Current Opinion in Neurology · doi:10.1097/00019052-199912000-00010 · Cited by 118
Self-citationIwata, A., Chen, X., McIntosh, T. K., Browne, K. D., & Smith, D. H. (2002) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/61.12.1056 · Cited by 116
Self-citationTraumatic Brain Injury, Neuroinflammation, and Post-Traumatic Headaches
Mayer, C. L., Huber, B., & Peskind, E. (2013) · Headache · doi:10.1111/head.12173 · Cited by 119
Graham, D., Raghupathi, R., Saatman, K., Meaney, D., & McIntosh, T. (2000) · Acta Neuropathologica · doi:10.1007/pl00007414 · Cited by 115
Self-citationRao, V. L. R., Dogan, A., Bowen, K., Todd, K., & Dempsey, R. J. (2001) · European Journal of Neuroscience · doi:10.1046/j.1460-9568.2001.01367.x · Cited by 115
Age-dependent synuclein pathology following traumatic brain injury in mice.
Uryu, K., Giasson, B. I., Longhi, L., Martinez, D., Murray, I. V. J., Conte, V., Nakamura, M., Saatman, K., Talbot, K., Horiguchi, T., et al. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00245-0 · Cited by 113
“Recognition of CCI-injured areas APP immunoreactivity (IR) was used to detect axons damaged by CCI in brain subjacent to the impact site as described (Pierce et al., 1998).”
Self-citationAnimal Models of Post-Traumatic Epilepsy
Pitkänen, A., & McIntosh, T. (2006) · Journal of Neurotrauma · doi:10.1089/neu.2006.23.241 · Cited by 112
“Based on published reports concerning long-term behavioral consequences of lateral FPI, we can assume that at least a subpopulation of our epileptic rats had impaired motor behavior (Pierce et al., 1998) and spatial memory (Browne et al., 2004).”
Self-citationBarrett, J. P., Henry, R. J., Shirey, K. A., Doran, S. J., Makarevich, O. D., Ritzel, R. M., Meadows, V. A., Vogel, S. N., Faden, A. I., Stoica, B. A., et al. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.2516-19.2020 · Cited by 129
“…addition, experimental models of repeated mild or moderate-to-severe TBI result in persistent brain inflammation and neurodegeneration leading to long-term motor and cognitive function deficits (Pierce et al., 1998; Dixon et al., 1999; Aungst et al., 2014; Loane et al., 2014; Mouzon et al., 2014).”
BackgroundChen, X., Iwata, A., Nonaka, M., Browne, K. D., & Smith, D. H. (2003) · Journal of Neurotrauma · doi:10.1089/089771503322144545 · Cited by 106
“…laboratories and ours have found that brain trauma in rats produces long-term neurodegenerative changes similar to those found in humans, including progressive brain atrophy, reactive astrocytosis, neuron death and axonal degeneration (Dixon et al, 1999; Pierce et al., 1998; Smith et al., 1997).”
Self-citationBrain injury, neuroinflammation and Alzheimer's disease
Breunig, J. J., Guillot‐Sestier, M., & Town, T. (2013) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2013.00026 · Cited by 106
Pischiutta, F., Micotti, E., Hay, J. R., Marongiu, I., Sammali, E., Tolomeo, D., Vegliante, G., Stocchetti, N., Forloni, G., Simoni, M. G. D., et al. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.11.003 · Cited by 122
“Abbreviations: AD, axial diffusivity; CC, corpus callosum; CCI, controlled cortical impact; cl, contralateral; CTE, chronic traumatic encephalopathy; CV, Cresyl violet; DTI, diffusion tensor imaging; EC, external capsule; EPI, echo-planar imaging; FA, fractional anisotropy; FPI, fluid percussion injury; il, ipsilatera…”
InfluentialSchuhmann, M., Stiller, D., Skardelly, M., Bernarding, J., Klinge, P., Samii, A., Samii, M., & Brinker, T. (2003) · Journal of Neurotrauma · doi:10.1089/089771503767869962 · Cited by 107
“In contrary, animal studies applying fluid-percussion or diffuse rotational injury, did not show any change in Cho up to 7 days post TBI (Cecil et al., 1998b; Rubin et al., 1997; Smith et al., 1998).”
Neuropathology of the vegetative state after head injury
Graham, D. I., Adams, J., Murray, L. S., & Jennett, B. (2005) · Neuropsychological Rehabilitation · doi:10.1080/09602010443000452 · Cited by 106
Inflammation in Traumatic Brain Injury
Postolache, T. T., Wadhawan, A., Can, A., Lowry, C. A., Woodbury, M., Makkar, H., Hoisington, A. J., Scott, A. J., Potocki, E., Benros, M. E., et al. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191150 · Cited by 154
Lin, K., Niu, K.-C., Tsai, K., Kuo, J., Wang, L., Chio, C., & Chang, C. (2012) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0b013e31823c575f · Cited by 112
Huh, J. W., Widing, A. G., & Raghupathi, R. (2007) · Journal of Neurotrauma · doi:10.1089/neu.2006.0072 · Cited by 73
“Manual shaking for 12 min followed by hypoxia for 5 min on 3 consecutive days in 6-day-old rats demonstrated evidence of cortical hemorrhage associated with free radical formation and atrophy of cortical tissue (Smith et al., 1998).”
Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury
Paternò, R., Folweiler, K. A., & Cohen, A. S. (2017) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-017-0762-x · Cited by 130
Rodriguez-Paez, A. C., Brunschwig, J. P., & Bramlett, H. M. (2005) · Acta Neuropathologica · doi:10.1007/s00401-005-1010-z · Cited by 94
“Atrophy of both gray and white matter structures after clinical and experimental traumatic brain injury (TBI) have been well documented [3, 7, 8, 9, 10, 20, 21, 70, 72, 79, 83].”
Osier, N. D., Carlson, S. W., DeSana, A. J., & Dixon, C. E. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2014.3680 · Cited by 114
“One of the studies found that deficits persisted out to 2 months postinjury.(27) The MWM, discussed below in relation to its use for assessment of cognitive”
BackgroundInfluentialBondi, C. O., Klitsch, K. C., Leary, J. B., & Kline, A. E. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2014.3328 · Cited by 101
Overview of Traumatic Brain Injury: An Immunological Context
Nizamutdinov, D., & Shapiro, L. A. (2017) · Brain Sciences · doi:10.3390/brainsci7010011 · Cited by 104
“It is often deduced that the neuropathology in these regions underlies the observed neurobehavioral and cognitive deficits that are commonly seen in the FPI model [36,49,50].”
BackgroundHead Injury, Alpha-Synuclein Rep1 and Parkinson’s Disease
Goldman, S., Kamel, F., Ross, G., Jewell, S., Bhudhikanok, G. S., Umbach, D., Marras, C., Hauser, R., Jankovic, J., Factor, S., et al. (2012) · Annals of Neurology · doi:10.1002/ana.22499 · Cited by 96
Immonen, R., Kharatishvili, I., Gröhn, H., Pitkänen, A., & Gröhn, O. (2009) · NeuroImage · doi:10.1016/j.neuroimage.2008.11.022 · Cited by 96
“In rats the cell death continues up to one year (Bramlett and Dietrich 2002; Pierce et al., 1998; Smith et al., 1997) and the corresponding time period in humans can be several years.”
Kline, A., Massucci, J., Ma, X.-C., Zafonte, R. D., & Dixon, C. E. (2004) · Journal of Neurotrauma · doi:10.1089/neu.2004.21.1712 · Cited by 95
“…attenuation of spatial learning acquisition deficits with BRO has significant relevance for human TBI considering that both clinical and experimental studies have demonstrated persistent cognitive impairments after brain injury (Levin et al., 1987, 1990; Pierce et al., 1998; Dixon et al., 1999a).”
Behavioral consequences of minimal traumatic brain injury in mice.
Zohar, O., Rubovitch, V., Milman, A., Schreiber, S., & Pick, C. G. (2011) · Acta Neurobiologiae Experimentalis · doi:10.55782/ane-2011-1821 · Cited by 93
“Studies utilizing various experimental models of TBI indicate that the primary brain damage triggers cellular pathologies, which in turn lead to long-lasting secondary neuronal and glial damage (Pierce et al. 1996, 1998, Berger et al. 1999, Graham et al. 2000, Albensi 2001).”
MethodWatson, D., Longhi, L., Lee, E. B., Fulp, C. T., Fujimoto, S. T., Royo, N., Passini, M., Trojanowski, J., Lee, V., McIntosh, T., et al. (2003) · Journal of Neuropathology and Experimental Neurology · doi:10.1093/jnen/62.4.368 · Cited by 93
Self-citationBrain Trauma in Aged Transgenic Mice Induces Regression of Established Aβ Deposits
Nakagawa, Y., Reed, L., Nakamura, M., McIntosh, T. K., Smith, D. H., Saatman, K. E., Raghupathi, R., Clemens, J., Saido, T. C., Lee, V. M.-Y., et al. (2000) · Experimental Neurology · doi:10.1006/exnr.2000.7375 · Cited by 91
Self-citationAnimal models of post-traumatic epilepsy.
Ostergard, T., Sweet, J., Kusyk, D., Herring, E., & Miller, J. P. (2016) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2016.03.023 · Cited by 90
Atomic Force Microscopy Reveals Important Differences in Axonal Resistance to Injury
Magdesian, M. H., Sanchez, F. S., Lopez, M., Thostrup, P., Durisic, N., Belkaïd, W., Liazoghli, D., Grütter, P., & Colman, D. (2012) · Biophysical Journal · doi:10.1016/j.bpj.2012.07.003 · Cited by 78
“Dynamic deformation of axons rarely leads to primary disconnection during brain trauma (1,4,39).”
BackgroundBareyre, F. M., Saatman, K. E., Raghupathi, R., & McIntosh, T. K. (2000) · Journal of Neurotrauma · doi:10.1089/neu.2000.17.1029 · Cited by 77
“To better Hicks et al., 1996; Pierce et al., 1998; Smith et al., 1997a). understand the mechanisms underlying histological dam-Several studies have evaluated the deleterious neuro-age associated with human head injury, a number of ex-chemical processes leading to neuronal cell death fol-perimental…”
Self-citationZlotnik, A. A., Синельников, И. Е., Gruenbaum, B. F., Gruenbaum, S. E., Dubilеt, M., Dubilet, E., Leibowitz, A., Ohayon, S., Regev, A., Boyko, M., et al. (2011) · Anesthesiology · doi:10.1097/aln.0b013e31823d7731 · Cited by 80
“Moreover, long-term investigations have found long-term neurologic dysfunction when using the latter model.(49) The applicability of treatment with blood glutamate scavengers in human subjects remains a major concern.”
BackgroundSaber, M., Kokiko‐Cochran, O. N., Puntambekar, S. S., Lathia, J. D., & Lamb, B. T. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2016.4401 · Cited by 97
Functional Assessment of Long-Term Deficits in Rodent models of Traumatic Brain Injury
Gold, E. M., Su, D., López-Velázquez, L., Haus, D. L., Perez, H. D., Lacuesta, G. A., Anderson, A. J., & Cummings, B. J. (2013) · Regenerative Medicine · doi:10.2217/rme.13.41 · Cited by 90
Rostami, E., Davidsson, J., Ng, K. C., Jia, L., Gyorgy, A. B., Walker, J., Wingo, D., Plantman, S., Bellander, B., Agoston, D. V., et al. (2012) · Frontiers in Neurology · doi:10.3389/fneur.2012.00115 · Cited by 93
“Persisted behavioral deficits following severe TBI has previously been reported in other TBI models (Pierce et al., 1998).”
Immonen, R., Kharatishvili, I., Niskanen, J., Gröhn, H., Pitkänen, A., & Gröhn, O. (2009) · Experimental Neurology · doi:10.1016/j.expneurol.2008.09.009 · Cited by 87
“The fact that all three measured parameters were so highly increased indicates a massive increase of the extracellular water content of the tissue, increasing amount of so called free water (that is, water molecules lacking interactions with surrounding macromolecules) reflecting the progressive loss of proteins in ex…”
BackgroundResultInfluentialOsteen, C. L., Giza, C. C., & Hovda, D. A. (2004) · Neuroscience · doi:10.1016/j.neuroscience.2004.06.034 · Cited by 92
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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