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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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Items 201–300 of 354
Carlson, S. W., & Dixon, C. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5509 · Cited by 34
Animal Models of Traumatically-Induced Dementia
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“, 2008) between the craniotomy model (Pierce et al., 1998; Hannay et al., 1999; Laurer and McIntosh, 1999; Royle et al., 1999; Williams et al., 2005) and minor head injury model (Tang et al.”
MethodImmonen, R. J., Heikkinen, T., Tähtivaara, L., Nurmi, A., Stenius, T.-K., Puoliväli, J. T., Tuinstra, T., Phinney, A. L., Vliet, B. J. V., Yrjänheikki, J., et al. (2010) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2010.15 · Cited by 34
In situ DNA fragmentation occurs in white matter up to 12 months after head injury in man
Williams, S. E., Raghupathi, R., MacKinnon, M., Mcintosh, T. K., Saatman, K., & Graham, D. I. (2001) · Acta Neuropathologica · doi:10.1007/s004010100410 · Cited by 33
“Recent experimental studies have suggested that cerebral atrophy after head injury is progressive [8, 17, 38 , 45] and reflects structural damage that occurred at the time of injury with subsequent progressive neurodegeneration.”
BackgroundSelf-citationShimamura, M., Garcia, J. M., Prough, D., Dewitt, D., Uchida, T., Shah, S. A., Avila, M. A., & Hellmich, H. L. (2005) · Neuroscience · doi:10.1016/j.neuroscience.2004.10.041 · Cited by 33
Neural Stem Cells as Biological Minipumps: A Faster Route to Cell Therapy for the CNS?
Chen, H.-C. I., Bakshi, A., Royo, N. C., Magge, S. N., Watson, D. J., Royo, N. C., Magge, S. N., & Watson, D. J. (2007) · Current Stem Cell Research & Therapy · doi:10.2174/157488807779317044 · Cited by 27
Mao, X., Terpolilli, N. A., Wehn, A. C., Cheng, S., Hellal, F., Liu, B., Şeker, F. B., & Plesnila, N. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2019.6510 · Cited by 41
“53 54–69 Recent promising studies already detected important roles for inflammatory processes 55,64,65 and cis -phosphorylated tau 62,66–68,70 In order to expand our knowledge about the chronic sequelae of TBI, the current study was therefore not only designed to evaluate histopathological…”
Folweiler, K. A., Samuel, S., Metheny, H. E., & Cohen, A. S. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5350 · Cited by 37
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“…also follow previous cross-sectional histological studies demonstrating ongoing pathology for up to 1 year, including chronic inflammation, neurodegeneration, and axonal injury (Bramlett et al., 1997; Smith et al., 1997; Pierce et al., 1998; Philips et al., 2001; Morganti-Kossmann et al., 2002).”
Klementiev, B., Novikova, T., Korshunova, I., Berezin, V., & Bock, E. (2008) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2008.06245.x · Cited by 31
“…injury and is characterized by morphologically evident brain damage, breakdown of the blood–brain barrier and formation of edema, and is accompanied by motor and cognitive disturbances (Pierce et al., 1998; Hannay et al., 1999; Laurer & McIntosh, 1999; Royle et al., 1999; Williams et al., 2005).”
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“In regards to the lack of hippocampal mediated cognitive impairment seen in this study, previous studies, contrastingly, have shown persistent cognitive deficits post-TBI, with, for example, Pearce et al observing significant deficits in spatial learning ability in the MWM beginning at two months and lasting up to one…”
Cell-Free DNA as a Marker for Prediction of Brain Damage in Traumatic Brain Injury in Rats
Ohayon, S., Boyko, M., Saad, A., Douvdevani, A., Gruenbaum, B., Melamed, I., Shapira, Y., Teichberg, V., & Zlotnik, A. (2012) · Journal of Neurotrauma · doi:10.1089/neu.2011.1938 · Cited by 30
“Moreover, studies have found long-term neurological dysfunction when using the latter model (Pierce et al., 1998).”
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“8,29 Apparently the cortical areas processing these functions (particularly the motor areas) did not undergo severe enough permanent damage after lateral FPI to cause an impairment in composite neuroscore.”
Persistent Behavioral Deficits in Rats after Parasagittal Fluid Percussion Injury
Sell, S. L., Johnson, K. M., DeWitt, D. S., & Prough, D. S. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2016.4616 · Cited by 33
“23 Arguably the most important outcome measure of a TBI model is behavior, as this is the best way to test meaningful brain function.”
Nudi, E., Jacqmain, J., Dubbs, K., Geeck, K., Salois, G., Searles, M. A., & Smith, J. S. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2014.3618 · Cited by 34
Phosphodiesterase Inhibition Rescues Chronic Cognitive Deficits Induced by Traumatic Brain Injury
Titus, D. J., Sakurai, A., Kang, Y., Furones, C., Jergová, S., Santos, R., Sick, T. J., & Atkins, C. M. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.5133-12.2013 · Cited by 80
“…and learning and memory deficits induced by TBI, we used the fluidpercussion brain injury model, a clinically relevant model of TBI that elicits reproducible deficits in hippocampal-dependent learning and memory (Dash et al., 1995; Bramlett et al., 1997a; Scheff et al., 1997; Pierce et al., 1998).”
Lotocki, G., Vaccari, J. P. D. R., Alonso, O., Molano, J. S., Nixon, R., Dietrich, W., & Bramlett, H. (2011) · Therapeutic Hypothermia and Temperature Management · doi:10.1089/ther.2010.0011 · Cited by 29
“The progressive nature of gray and white matter vulnerability after TBI (Pierce et al. , 1998; Dixon et al. , 1999; Bramlett and Dietrich, 2002) has been emphasized in experimental and clinical literature.”
Marklund, N., Keck, C. A., Hoover, R., Soltesz, K. M., Millard, M., Lebold, D., Spangler, Z. P., Banning, A., Benson, J., & McIntosh, T. (2005) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-2005-00287 · Cited by 29
“Although some recovery occurs in days to weeks following lateral FP brain injury, marked neurological motor function deficits are observed up to a year in this model [61].”
Self-citationInjury Severity and Sensitivity to Treatment After Controlled Cortical Impact in Rats
Markgraf, C. G., Clifton, G. L., Aguirre, M., Chaney, S. F., Bois, C. K., Kennon, K., & Verma, N. (2001) · Journal of Neurotrauma · doi:10.1089/08977150150502604 · Cited by 28
“While this pattern is observed to occur in many human brain injury patients, in a fluid percussion model of TBI, motor and cognitive deficits have both been found to persist for periods of up to a year (Pierce et al., 1998).”
Shishido, H., Ueno, M., Sato, K., Matsumura, M., Toyota, Y., Kirino, Y., Tamiya, T., Kawai, N., & Kishimoto, Y. (2019) · Behavioural Neurology · doi:10.1155/2019/3248519 · Cited by 30
Lithium increases hippocampal SNARE protein abundance after traumatic brain injury
Carlson, S. W., Yan, H. Q., & Dixon, C. E. (2016) · Experimental Neurology · doi:10.1016/j.expneurol.2016.12.006 · Cited by 28
“Lithium increases the abundance of CSPα mRNA and protein in the naïve rat brain, but not SNAP-25, syntaxin 33 and 35, α-synuclein, or synaptophysin abundance (Cordeiro et al., 2000, 2003; Scarr and Dean, 2012).”
BackgroundLeconte, C., Benedetto, C., Lentini, F., Simon, K., Ouaazizi, C., Taib, T., Cho, A. H., Plotkine, M., Mongeau, R., Marchand‐Leroux, C., et al. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2019.6679 · Cited by 37
“38 Another interesting finding here was the ipsilateral cell loss in the cingular cortex 5 months after TBI, and the reduced density of myelin fiber in the ipsilateral cingulum, 10 months after TBI.”
InfluentialRoyo, N., Lebold, D., Magge, S. N., Chen, I., Hauspurg, A., Cohen, A. S., & Watson, D. (2007) · Neuroscience · doi:10.1016/j.neuroscience.2007.06.014 · Cited by 27
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BackgroundMethodInfluentialChuang, C.-H., Hsu, Y., Wang, C.-C., Hu, C.-Y., & Kuo, J.-R. (2013) · Acupuncture in Medicine · doi:10.1136/acupmed-2013-010406 · Cited by 26
Delayed Changes in Regional Brain Energy Metabolism following Cerebral Concussion in Rats
Buczek, M., Alvarez, J., Azhar, J., Zhou, Y., Lust, W., Selman, W., & Ratcheson, R. (2002) · Metabolic brain disease · doi:10.1023/a:1019973921217 · Cited by 26
“…that the integrity of the BBB is compromised, edema formation peaks, neuroscores are depressed maximally, glial proliferation is significantly reduced, and caspase 8 expression is increased (Beeret al., 2001; Hill-Felberget al., 1999; Pierce et al., 1998; Shapiraet al., 1993; Soareset al., 1992).”
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“For example, neurological motor deficits have been reported after lateral FP injury, which, like in the clinical setting, persist for up to 1 year after injury (Mclntosh et al., 1989; Brown and Nell, 1992; Pierce et al., 1998; Swaine and Sullivan, 1996).”
Cognitive Impairment following Traumatic Brain Injury
Whiting, M. D., Baranova, A., & Hamm, R. J. (2006) · doi:10.1201/9781420004335.ch14 · Cited by 26
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“The development of neurobehavioral dysfunction following lFPI replicates the motor and cognitive impairments clinically reported by individuals afflicted with a TBI (3, 44).”
Neuroimaging and traumatic brain injury: State of the field and voids in translational knowledge.
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Lateralized Response of Dynorphin A Peptide Levels after Traumatic Brain Injury
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“Damage to the hippocampus may account for injury-related cognitive impairment (Bramlett et al., 1997; Colicos et al., 1996; Pierce et al., 1998).”
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“Traumatic brain injury (TBI) in rats leads to chronic neuronal death in the hippocampus that continues for almost a year after the impact (Smith et al., 1997; Pierce et al., 1998; Dixon et al., 1999).”
BackgroundPassineau, M., Zhao, W.-Z., Busto, R., Dietrich, W., Alonso, O., Loor, J. Y., Bramlett, H., & Ginsberg, M. (2000) · American Journal of Physiology. Heart and Circulatory Physiology · doi:10.1152/ajpheart.2000.279.3.h924 · Cited by 25
López-Preza, F. I., de la Cruz, S. H., Santiago-Castañeda, C., Silva‐Velasco, D. L., Beltran‐Ornelas, J. H., Tapia-Martínez, J. A., Sánchez‐López, A., Rocha, L., & Centurión, D. (2022) · Life Sciences · doi:10.1016/j.lfs.2022.121218 · Cited by 25
Neuroprotective effect of lithium in cold- induced traumatic brain injury in mice.
Çiftçi, E., Karacay, R., Caglayan, A., Altunay, S., Ates, N., Altintas, M., Doeppner, T., Yuluğ, B., & Kılıç, E. (2020) · Behavioural Brain Research · doi:10.1016/j.bbr.2020.112719 · Cited by 24
Lippert-Gruener, M., Maegele, M., Garbe, J., & Angelov, D. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2006.07.025 · Cited by 24
Zaltsman, S. L., Friedman‐Levi, Y., Shabashov-Stone, D., Gincberg, G., Atrakcy-Baranes, D., Joy, M. T., Carmichael, S. T., Silva, A. J., & Shohami, E. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2020.7015 · Cited by 34
Correa, F. G., Hetzer, S. M., Shalosky, E. M., Goodman, M. D., & Evanson, N. K. (2019) · Journal of Neuroscience Research · doi:10.1002/jnr.24535 · Cited by 21
Alam, S., Réhman, S. U., & Kim, M. O. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8020271 · Cited by 22
de la Tremblaye, P. B., O’Neil, D. A., LaPorte, M. J., B, J. P. C. A., Beitchman, J. A., Thomas, T. C., Bondi, C. O., & Kline, A. E. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.05.022 · Cited by 25
Li, S.-H., Kuroiwa, T., Katsumata, N., Ishibashi, S., Sun, L.-Y., Endo, S., & Ohno, K. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20720 · Cited by 22
“…memory and learning (Olton et al., 1979; Morris et al., 1982), it has been generally and widely accepted that selective neuronal death in the hippocampus plays a key role in cognitive dysfunction following TBI (Smith et al., 1994; Pierce et al., 1998; Floyd et al., 2002; Kline et al., 2002).”
BackgroundResultInfluentialAnimal Models of Movement Disorders
Lane, E., & Dunnett, S. (2012) · Neuromethods · doi:10.1007/978-1-61779-298-4 · Cited by 22
“Conversely, glutamate levels within the striatum – and the sensorimotor cortex – have been shown to be higher on the side contralateral to an active, compared to an immobilised limb, and studies have indicated that the exclusive use of a limb can exaggerate the extent of tissue damage in rodent stroke model (61, 62),…”
BackgroundInfluentialThe evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies
Zima, L. A., Moore, A. N., Smolen, P. D., Kobori, N., Noble, B., Robinson, D., Hood, K. N., Homma, R., Mamun, A. A., Redell, J. B., et al. (2024) · Neurochemistry International · doi:10.1016/j.neuint.2024.105874 · Cited by 21
Chronic Cognitive and Cerebrovascular Function after Mild Traumatic Brain Injury in Rats
Griffiths, D. R., Law, L., Young, C., Fuentes, A., Truran, S., Karamanova, N., Bell, L., Turner, G., Emerson, H. M., Mastroeni, D., et al. (2022) · bioRxiv · doi:10.1089/neu.2022.0015 · Cited by 21
“11,12 Pre-clinical studies in severe TBI show late (1-year) development of cognitive impairment following injury, 16–19 but empiric evidence as regards chronic consequence of mTBI is lacking.”
Neurogranin Protein Expression Is Reduced after Controlled Cortical Impact in Rats
Svirsky, S. E., Henchir, J. J., Li, Y.-M., Ma, X.-C., Carlson, S. W., & Dixon, C. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6759 · Cited by 21
Yasmin, A., Pitkänen, A., Jokivarsi, K., Poutiainen, P., Gröhn, O., & Immonen, R. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00863 · Cited by 21
“Sustained thalamic inflammation and associated reactive gliosis is well documented in this animal model (Pierce et al., 1998; Lehto et al., 2012), and in human TBI (Papadopoulos and Lecanu, 2009; Ramlackhansingh et al.”
BackgroundWang, C.-C., Wee, H.-Y., Hu, C.-Y., Chio, C., & Kuo, J. (2018) · World Neurosurgery · doi:10.1016/j.wneu.2018.01.140 · Cited by 22
Altered Effective Connectivity of Hippocampus-Dependent Episodic Memory Network in mTBI Survivors
Yan, H. J., Feng, Y., & Wang, Q. (2016) · Neural Plasticity · doi:10.1155/2016/6353845 · Cited by 20
Jacqmain, J., Nudi, E., Fluharty, S., & Smith, J. S. (2014) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.08.056 · Cited by 24
Genetic predictors of outcome following traumatic brain injury
Lipsky, R. H., & Lin, M. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-52892-6.00003-9 · Cited by 26
Abikenari, M. A., Ha, J. H., Liu, J., Ren, A. L., Cho, K. B., Lim, J., Kim, L. H., Medikonda, R. T., Choi, J. H., & Lim, M. K. (2025) · Frontiers in Neurology · doi:10.3389/fneur.2025.1668480 · Cited by 18
Identifying the Phenotypes of Diffuse Axonal Injury Following Traumatic Brain Injury
Krieg, J. L., Leonard, A. V., Turner, R. J., & Corrigan, F. (2023) · Brain Sciences · doi:10.3390/brainsci13111607 · Cited by 24
“More severe injury, like the focal CCI model, produces more chronic APP axonal pathology, detected from one month to one year post-injury in white matter and grey matter structures like the striatum and thalamus [97].”
BackgroundQuantitative susceptibility mapping of the rat brain after traumatic brain injury
Chary, K., Nissi, M. J., Nykänen, O., Manninen, E., Rey, R. I., Shmueli, K., Sierra, A., & Gröhn, O. (2020) · NMR in Biomedicine · doi:10.1002/nbm.4438 · Cited by 38
Animal Models of Post-Traumatic Epilepsy
Keith, K. A., & Huang, J. H. (2019) · Diagnostics · doi:10.3390/diagnostics10010004 · Cited by 26
“Furthermore, FPI model demonstrates persistent neuromotor and cognitive deficits up to one year following severe FPI with the associated temporal pattern of cellular death that recapitulate what is seen in traumatic brain injury patient [26,27].”
BackgroundArulsamy, A., Corrigan, F., & Collins‐Praino, L. E. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.02.045 · Cited by 21
Huh, J. W., Widing, A. G., & Raghupathi, R. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2010.1639 · Cited by 19
“…effects on brain morphology alterations following graded contusive trauma have not been evaluated in either adult or immature rodents, our data support previous reports of increased tissue loss and ventricular enlargement in adult rats over a 1-year period (Dixon et al., 1999; Pierce et al., 1998).”
BackgroundResultPillay, N., Kellaway, L. A., & Kotwal, G. (2007) · Brain Research · doi:10.1016/j.brainres.2007.03.056 · Cited by 19
Injury Models of the Central Nervous System
Kobeissy, F., Dixon, C., Hayes, R., & Mondello, S. (2016) · Methods in Molecular Biology · doi:10.1007/978-1-4939-3816-2 · Cited by 19
Fronczak, K. M., Li, Y., Henchir, J., Dixon, C. E., & Carlson, S. W. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02534-3 · Cited by 18
“Patients and clinical reports indicate that persistent cognitive dysfunction can greatly contribute to reduced quality of life of individuals living with a TBI, across the spectrum of injury severity [1-6].”
BackgroundKoch, P. F., Cottone, C., Adam, C. D., Ulyanova, A. V., Russo, R. J., Weber, M. T., Arena, J. D., Johnson, V. E., & Wolf, J. A. (2020) · eNeuro · doi:10.1523/eneuro.0495-19.2020 · Cited by 23
“H&E staining revealed a focal intraparenchymal lesion consistent with previous descriptions of the model (Pierce et al., 1998).”
Enduring Neuroprotective Effect of Subacute Neural Stem Cell Transplantation After Penetrating TBI
Kassi, A., Mahavadi, A. K., Clavijo, A., Caliz, D., Lee, S. W., Ahmed, A. I., Yokobori, S., Hu, Z., Spurlock, M. S., Wasserman, J. M., et al. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2018.01097 · Cited by 20
Karver, C. L., Wade, S. L., Cassedy, A. E., Taylor, H. G., Brown, T. M., Kirkwood, M. W., & Stancin, T. (2013) · Child Neuropsychology · doi:10.1080/09297049.2013.796918 · Cited by 21
Tomasevic, G., Laurer, H. L., Mattiasson, G., Steeg, H., Wieloch, T. W., & McIntosh, T. K. (2012) · Journal of neurosurgery · doi:10.3171/2012.2.jns11888 · Cited by 18
Self-citationHeiskanen, M., Jääskeläinen, O., Manninen, E., Gupta, S. D., Andrade, P., Ciszek, R., Gröhn, O., Herukka, S., Puhakka, N., & Pitkänen, A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232315208 · Cited by 17
“The present study investigated whether rat plasma NF-L levels predict structural and behavioral outcomes and post-traumatic epileptogenesis after lateral FPI-induced TBI.”
ResultInfluentialManninen, E., Chary, K., Lapinlampi, N., Andrade, P., Paananen, T., Sierra, A., Tohka, J., Gröhn, O., & Pitkänen, A. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6796 · Cited by 17
Ndode-Ekane, X., Matthiesen, L., Banuelos-Cabrera, I., Palminha, C., & Pitkänen, A. (2018) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-170811 · Cited by 17
“We focused the analysis on the chronic time-points (30 d and 90 d post-injury), because, the inflammatory response at this phase is related to the progression of secondary damage (Hay et al., 2015; Pierce et al., 1998).”
Improving on Laboratory Traumatic Brain Injury Models to Achieve Better Results
Nyanzu, M. K., Siaw-Debrah, F., Ni, H., Xu, Z., Wang, H. X., Lin, X., Zhuge, Q., & Huang, L. (2017) · International Journal of Medical Sciences · doi:10.7150/ijms.18075 · Cited by 20
Delayed glucose treatment improves cognitive function following fluid-percussion injury.
Kokiko-Cochran, O., Michaels, M., & Hamm, R. J. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.02.046 · Cited by 17
Laurer, H., Meaney, D., Margulies, S., & McIntosh, T. (2002) · Elsevier eBooks · doi:10.1016/b0-12-227210-2/00211-9 · Cited by 17
Self-citationBriones, T. L. (2015) · Annual Review of Nursing Research · doi:10.1891/0739-6686.33.31 · Cited by 16
Novel therapies for combating chronic neuropathological sequelae of TBI
Ikonomović, M. D., Abrahamson, E. E., Carlson, S. W., Graham, S. H., & Dixon, C. E. (2018) · Neuropharmacology · doi:10.1016/j.neuropharm.2018.06.021 · Cited by 16
“Four chronic (~12-month) studies reported deficits in neurological scores and spatial memory (Dixon et al., 1999; Meehan et al., 2012; Pierce et al., 1998; Shelton et al., 2008).”
Axonal Damage due to Traumatic Brain Injury
Saatman, K. E., Serbest, G., & Burkhardt, M. F. (2008) · Springer eBooks · doi:10.1007/978-0-387-30375-8_16 · Cited by 8
Gozt, A., Hellewell, S. C., Ward, P. G. D., Bynevelt, M., & Fitzgerald, M. (2021) · Neuroscience · doi:10.1016/j.neuroscience.2021.05.030 · Cited by 16
Maqbool, J., Anwar, H., Iqbal, J., Rasul, A., Imran, A., Malik, S. A., Shabbir, A., Ijaz, F., Sajid, F., Akram, R., et al. (2020) · Food Science & Nutrition · doi:10.1002/fsn3.2033 · Cited by 14
Zheng, F., Zhou, Y.-T., Li, P.-F., Hu, E., Li, T., Tang, T., Luo, J.-K., Zhang, W., Ding, C.-S., & Wang, Y. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00876 · Cited by 14
“Although cortical and hippocampal metabolomics studies of acute and chronic TBI were well documented (Pierce et al., 1998; Casey et al., 2008; McGuire et al., 2019), we believe that a description on metabolomics of subacute TBI remains urgent.”
BackgroundLim, S.-W., Tt, E. N., Hu, C.-Y., Chio, C., Wang, C.-C., & Kuo, J.-R. (2018) · World Neurosurgery · doi:10.1016/j.wneu.2018.01.036 · Cited by 14
Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Smith, C. J., Johnson, B. N., Elkind, J. A., See, J., Xiong, G., & Cohen, A. (2012) · Journal of Visualized Experiments · doi:10.3791/4411 · Cited by 14
Lifshitz, J., & McIntosh, T. K. (2003) · Journal of Neurotrauma · doi:10.1089/08977150360547062 · Cited by 11
“Damage to mtDNA may therefore contribute to the ongoing pathology and behavioral deficits associated with TBI (Smith et al., 1997; Pierce et al., 1998), resembling the proposed mechanisms underlying normal aging.”
Self-citationTomasevic, G., Raghupathi, R., Scherbel, U., Wieloch, T. W., & McIntosh, T. K. (2010) · Journal of Neuroscience Research · doi:10.1002/jnr.22491 · Cited by 12
“TBI results in neuronal cell loss, both in the acute posttraumatic phase and in a more progressive fashion, termed delayed neuronal death (DND; Pierce et al., 1998).”
BackgroundSelf-citationTraumatic brain injury in late adolescent rats: Effects on adulthood memory and anxiety.
Amorós-Aguilar, L., Portell-Cortés, I., Costa‐Miserachs, D., Torras-García, M., & Coll-Andreu, M. (2015) · Behavioral Neuroscience · doi:10.1037/bne0000046 · Cited by 15
“…of spatial memory deficits has been reported after LFP over periods of weeks (Bramlett, Green, & Dietrich, 1997), and even up to one year (Pierce et al., 1998), but there is one report indicating that the memory deficits found in the first month after the initial damage were no longer…”
BackgroundStatistical Issues in TBI Clinical Studies
Rapp, P. E., Cellucci, C. J., Keyser, D. O., Gilpin, A. M. K., & Darmon, D. M. (2013) · Frontiers in Neurology · doi:10.3389/fneur.2013.00177 · Cited by 15
“In rats, progressive loss of brain tissue and deterioration of cognitive performance can continue for a year following injury (58, 61, 62).”
BackgroundCholinergic Treatment of Traumatic Brain Injury
Tenovuo, O. S. (2006) · Current Drug Therapy · doi:10.2174/157488506776930932 · Cited by 14
Maegele, M., Braun, M., Wafaisade, A., Schäfer, N., Lippert-Gruener, M., Kreipke, C., Rafols, J., Schäfer, U., Angelov, D., & Stuermer, E. (2015) · Physiological Research · doi:10.33549/physiolres.932664 · Cited by 12
“Within the first week after injury, EE animals recovered significantly some neurological function (EE 15.2±1.4) while animals held under standard housing displayed a worsening with respect to their neurofunction (SH 10.2±0.9) (Fig.”
BackgroundMethodResultInfluentialMany roads to Parkinson’s disease neurodegeneration: Head trauma- A road more traveled than we know?
Irwin, D. J., & Trojanowski, J. (2013) · Movement Disorders · doi:10.1002/mds.25551 · Cited by 11
“These include the presence of abnormal protein aggregations(23) of tau, Ab, and alpha-syn with long-term neuropathological(27,28) and clinical sequelae.(27) Axonal injury results in accumulation of amyloid-precursor protein (APP) within hours in terminal axonal retraction bulbs, accompanied by the end-product protein,…”
BackgroundSelf-citationKotwal, G., Lahiri, D., & Hicks, R. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04659.x · Cited by 11
Mechanical mechanism and indicator of diffuse axonal injury under blast-type acceleration
Du, Z., Wang, P., Luo, P., Zhou, F., Zhuang, Z., & Liu, Z. (2023) · Journal of Biomechanics · doi:10.1016/j.jbiomech.2023.111674 · Cited by 10
Stelfa, G., Švalbe, B., Vavers, E., Dūrītis, I., Dambrova, M., & Zvejniece, L. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.985895 · Cited by 13
“Only one study showed that hippocampal-dependent learning tasks were affected from 2 to 12 months after latFPI in rats; however, the injury was accompanied by progressive tissue loss resembling severe brain injury (18).”
BackgroundAnimal models of post-traumatic epilepsy and their neurobehavioral comorbidities.
Santana-Gomez, C., Medel-Matus, J.-S., & Rundle, B. (2021) · Seizure · doi:10.1016/j.seizure.2021.05.008 · Cited by 10
Beitchman, J. A., Lifshitz, J., Harris, N., Thomas, T. C., Lafrenaye, A. D., Hånell, A., Dixon, C. E., Povlishock, J., & Rowe, R. K. (2020) · bioRxiv · doi:10.1089/neur.2020.0046 · Cited by 10
“Cognitive performance is degraded in short, long, and working memory, using various cognitive testing modalities [10, 32, 35-45].”
BackgroundMethodHaar, C. V., & Winstanley, C. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4276 · Cited by 10
Keck, C. A., Thompson, H., Pitkänen, A., Lebold, D., Morales, D., Plevy, J. B., Puri, R., Zhao, B., Dichter, M., & McIntosh, T. (2007) · Restorative Neurology and Neuroscience · doi:10.3233/rnn-2007-00370 · Cited by 10
“Neuronal cell death begins almost immediately following the injury and has been shown to continue for up to a year (Pierce, et al., 1998; Smith, Chen, Pierce, et al., 1997).”
Self-citationKaniuk, J. K., Kumar, D., Mazurek, C. Y., Khavari, S., Sollenberger, C. H., Ahuja, A., Mossner, J. M., & Ahuja, C. S. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157191 · Cited by 11
“Various animal studies have demonstrated both STM and long-term memory deficits following TBI, sometimes lasting for year [99,100].”
Srinivasan, G. R., & Brafman, D. A. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.813544 · Cited by 10
“With respect to amyloid-related phenotypes, increased APP immunoreactivity, a marker of axonal damage has been observed in the white matter in rats acutely (Ciallella et al., 2002) as well as chronically (Pierce et al., 1998; Acosta et al., 2017) (up to 1 year) post-injury.”
BackgroundPrajapati, P., Wang, W., Pesina, S. A., Geleta, U., & Springer, J. E. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-021-01164-6 · Cited by 10
“1 3 dynamic changes of pro- and anti-inflammatory miRNAs is consistent with the experimental and clinical observations that while reparative anti-inflammatory signaling peak shortly following brain injury, pro-inflammatory effectors persist for weeks to months to years (Loane et al. 2014; Pierce et al. 1998).”
BackgroundResultAravind, A., Kosty, J., Chandra, N., & Pfister, B. J. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113378 · Cited by 11
Segovia-Oropeza, M., Santiago-Castañeda, C. L., Orozco-Suárez, S., Concha, L., & Rocha, L. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6975 · Cited by 9
“10,33,54 The present results demonstrate that animals receiving subchronic CG treatment after severe TBI show lower sensorimotor dysfunction, which was reversed within 30 days post-trauma.”
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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