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Immunohistochemical characterization of alterations in the distribution of amyloid precursor proteins and beta-amyloid peptide after experimental brain injury in the rat
Open accessAbstract
Recent reports suggest a relationship between traumatic brain injury and the precocious development of neurodegenerative cascades, including diffuse deposits of beta-amyloid peptides (A beta) in the injured brain. Because the lateral fluid-percussion (FP) model of experimental brain injury produces clinically relevant neuropathological sequelae in the rat brain, we used this model together with a series of antibodies specific for amyloid precursor proteins (APPs), APP-like proteins (APLPs), or A beta to identify acute neurodegenerative changes after brain trauma. Male Sprague-Dawley rats were anesthetized and subjected to lateral FP brain injury of moderate to high severity. At 1 hr, 2 hr, 48 hr, 1 week, or 2 weeks after injury, animals were killed and their brains were removed for immunohistochemical analysis. APP/APLP immunoreactivity increased in specific brain regions as early as 1 hr after injury and persisted for at least 2 weeks. Axons in the thalamus and subcortical white matter showed the greatest APP/APLP accumulation. Injured cortex, striatum, cingulum, and hippocampus also demonstrated significant axonal accumulations of APP/APLP. Accumulation of APP/APLPs occurred primarily ipsilateral to the injury, although bilateral changes were observed in some brain regions. No deposition of A beta was observed in any brain region at any time point examined. These results demonstrate a pattern of widespread axonal pathology after lateral FP brain injury in the rat, characterized by intra-axonal accumulations of APP/APLP immunoreactivity in the absence of plaque- like deposits of A beta in the traumatized brain.
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“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 [121]
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“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 [121]
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Citations
Cites
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
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“One such transgenic mouse expressing human APP developed spontaneous deposits of A/3 that form amyloid fibrils (Games et al., 1995).”
BackgroundDiffuse axonal injury and traumatic coma in the primate
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BackgroundSelf-citationTraumatic brain injury in the rat: characterization of a lateral fluid-percussion model.
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“Our laboratory has established a model of experimental lateral fluid-percussion (FP) brain injury in the rat (McIntosh et al., 1989) that produces reproducible and clinically relevant his- topathological changes, including extensive neuronal loss and degeneration accompanied by gliosis in cortical…”
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“Because APP undergoes fast axonal transport (Koo et al., 1990), intra-axonal accumulations of APP/APLP may serve as earlier, highly specific markers of DA1 compared with other axonal proteins (e.”
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BackgroundMethodInfluentialSelf-citationTraumatically Induced Axonal Injury: Pathogenesis and Pathobiological Implications
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Cited by
Sorted by citations
Items 101–200 of 215
Ai, J., Liu, E., Wang, J.-L., Chen, Y.-H., Yu, J. L., & Baker, A. (2007) · Journal of Neurotrauma · doi:10.1089/neu.2006.0224 · Cited by 59
“…of axonal transport proteins in swollen regions of axons is the clear sign of damage to the axonal cytoskeleton, which is responsible for the transport (Yaghmai and Povlishock, 1992; Grady et al., 1993; Pierce et al., 1996; Sherriff et al., 1994; Gentleman et al., 1993; Blumbergs et al., 1995).”
Monitoring of β-Amyloid Dynamics after Human Traumatic Brain Injury
Marklund, N., Farrokhnia, N., Hånell, A., Vanmechelen, E., Enblad, P., Zetterberg, H., Blennow, K., & Hillered, L. (2013) · Journal of Neurotrauma · doi:10.1089/neu.2013.2964 · Cited by 64
“5,11,12 16 APP may be proteolytically cleaved by different enzymes including a -secretase, preventing the generation of A b peptides, or the b -site APP cleaving enzyme 1 (BACE1).”
Pugliese, M., Mascort, J., Mahy, N., & Ferrer, I. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0087-3 · Cited by 60
Maegele, M., Lippert‐Gruener, M., Ester‐Bode, T., Sauerland, S., Schäfer, U., Molčányi, M., Lefering, R. L., Bouillon, B., Neiss, W. F., Angelov, D. N., et al. (2005) · Journal of Neurotrauma · doi:10.1089/neu.2005.22.772 · Cited by 58
“Neuromotor and cognitive dysfunction has also been reported following experimental lateral fluid percussion brain injury (McIntosh et al., 1989a; Lyeth et al., 1990; Smith et al., 1991; Dietrich et al., 1996; Pierce et al., 1996).”
InfluentialSelf-citationMaegele, M., Lippert-Gruener, M., Ester-Bode, T., Garbe, J., Bouillon, B., Neugebauer, E., Klug, N., Lefering, R., Neiss, W., & Angelov, D. (2005) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2005.04070.x · Cited by 58
“Using the lateral fluid percussion (LFP) model in rats (Dixon et al., 1987; McIntosh et al., 1989; Dietrich et al., 1996; Pierce et al., 1996), several investigators have described the major histopathological consequences to trauma: (i) lesion-induced vascular perturbations (Cortez et al., 1989;…”
BackgroundResultInfluentialKasturi, B. S., & Stein, D. G. (2009) · Journal of Neurotrauma · doi:10.1089/neu.2008.0751 · Cited by 57
“…could be upstream precursors of other pathological lesions observed post-TBI—e.g., the deposition of beta-amyloid and = or amyloid precursor proteins in the cortical regions or the neuronal loss reported in an experimental model of TBI (Lewen et al., 1995; Pierce et al., 1996; Iwata et al., 2002).”
Ayton, S., Zhang, M., Roberts, B. R., Lam, L. Q., Lind, M., McLean, C., Bush, A. I., Frugier, T., Crack, P. J., & Duce, J. A. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.01.041 · Cited by 56
“hemorrhage is a feature of the TBI-effected brain [6, 7] and parallel studies have shown alterations in APP and CP post TBI[20-22].”
BackgroundResultAxonal Injury Is Accentuated in the Caudal Corpus Callosum of Head-Injured Patients
Leclercq, P., McKenzie, J., Graham, D. I., & Gentleman, S. (2001) · Journal of Neurotrauma · doi:10.1089/089771501750055721 · Cited by 56
“…lesions in human white matter (Nukina et al., 1992; Suenaga et al., 1994) and in a number of animal models of head injury (Lewen et al., 1995; Pierce et al., 1996; Bramlett et al., 1997; Smith et al., 1999; Graham et al., 2000), ischaemia (Kalaria et al., 1993), and cerebral infarction (Yam…”
Self-citationMarklund, N., Fulp, C. T., Shimizu, S., Puri, R., McMillan, A., Strittmatter, S., & McIntosh, T. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2005.08.029 · Cited by 54
“…diffuse axonal injury (DAI), is an important contributor to the morbidity and mortality seen both clinically and in experimental TBI (Adams et al., 1989; Pierce et al., 1996; Maxwell et al., 1997; Christman et al., 1997), and is characterized by axonal swelling and, ultimately, disconnection.”
BackgroundSelf-citationInduction of presenilins in the rat brain after middle cerebral arterial occlusion
Pennypacker, K. R., Hernandez, H., Benkovic, S. A., Morgan, D., Willing, A. E., & Sanberg, P. R. (1999) · Brain Research Bulletin · doi:10.1016/s0361-9230(99)00031-3 · Cited by 49
Update on TBI and Cognitive Impairment in Military Veterans
Elder, G. A. (2015) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-015-0591-8 · Cited by 56
Pathophysiology of Sports-Related Concussion
Giza, C. C., & DiFiori, J. P. (2010) · Sports Health A Multidisciplinary Approach · doi:10.1177/1941738110391732 · Cited by 64
“Two paradigms related to postinjury neural activation following concussive injury in the rat are reviewed here, and they provide insight to mechanisms of recovery after TBI.”
BackgroundInfluentialKe, C.-S., Poon, W., Ng, H.-K., Lai, F. M., Tang, N., & Pang, J. C. (2002) · Experimental Neurology · doi:10.1006/exnr.2002.8037 · Cited by 51
Clarke, J., Thornell, A., Corbett, D., Soininen, H., Hiltunen, M., & Jolkkonen, J. (2007) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2007.05807.x · Cited by 50
“Numerous studies have noted that APP expression is transiently increased following brain injury (Pierce et al., 1996) or ischaemia (Kim et al., 1998; Shi et al., 2000; Luan et al., 2005).”
BackgroundLonghi, L. G., Saatman, K. E., Raghupathi, R., Laurer, H. L., Lenzlinger, P. M., Riess, P., Neugebauer, E. A. M., Trojanowski, J. Q., Lee, V. M. ‐., Grady, M. S., et al. (2001) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1097/00004647-200111000-00001 · Cited by 51
“Traumatic brain injury in humans and rodents induces accumulation of APP in perikarya of neurons and in damaged axons (Pierce et al., 1996; Bramlett et al., 1997; Sheriff et al., 1994).”
Self-citationKhaksari, M., Soltani, Z., & Shahrokhi, N. (2017) · Translational Stroke Research · doi:10.1007/s12975-017-0588-5 · Cited by 50
“precursor protein to show early and progressive axonal damage and determine Valerian degeneration [91, 92].”
Kokiko-Cochran, O., Ransohoff, L., Veenstra, M., Lee, S., Saber, M., Sikora, M., Teknipp, R., Xu, G., Bemiller, S., Wilson, G., et al. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.3970 · Cited by 49
Animal models of closed-skull, repetitive mild traumatic brain injury
Hoogenboom, W. S., Branch, C. A., & Lipton, M. L. (2019) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2019.02.016 · Cited by 59
Estrone Is Neuroprotective in Rats after Traumatic Brain Injury
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“This increase in APP results in significant axonal injury, disruption of axonal transport, and neurodegeneration (Blasko et al., 2004; Bramlett et al., 1997; Ciallella et al., 2002; Lewen et al., 1995,1996; Otsuka et al., 1991; Pierce et al., 1996).”
BackgroundAmyloid Precursor Protein Revisited
Guo, Q.-X., Li, H., Gaddam, S. S., Justice, N., Robertson, C., & Zheng, H. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.315051 · Cited by 48
“The punctate APP staining following TBI is likely due to its accumulation in the damaged neuronal axons (14, 15).”
BackgroundAcute axonal damage in three different murine models of multiple sclerosis: A comparative approach
Höflich, K. M., Beyer, C., Clarner, T., Schmitz, C., Nyamoya, S., Kipp, M., & Hochstrasser, T. (2016) · Brain Research · doi:10.1016/j.brainres.2016.08.048 · Cited by 46
“It is also unclear whether loss of APP-immunoreactivity relates to degradation of the damaged axon and thus degradation of APP or whether at least some APPþ axons undergo regeneration (Bramlett et al., 1997; Pierce et al., 1996).”
Neurodegenerative pathways as targets for acquired epilepsy therapy development
Casillas-Espinosa, P. M., Ali, I. Y., & O'Brien, T. J. (2020) · Epilepsia Open · doi:10.1002/epi4.12386 · Cited by 59
Büchele, F., Morawska, M. M., Schreglmann, S. R., Penner, M., Muser, M. H., Baumann, C. R., & Noaín, D. (2015) · Journal of Neurotrauma · doi:10.1089/neu.2015.4001 · Cited by 54
“47 In rodent animal models, it has mainly been described for focal TBI 48,49 and inertial brain injury, 50 whereas evidence from models of diffuse TBI is scarce.”
Amyloid precursor protein requires the insulin signaling pathway for neurotrophic activity.
Wallace, W. C., Akar, C. A., Lyons, W. E., Kole, H., Egan, J. M., & Wolozin, B. (1997) · Brain Research. Molecular Brain Research · doi:10.1016/s0169-328x(97)00259-3 · Cited by 46
REVIEW ■ : Calcium and the Pathogenesis of Traumatic CNS Injury: Cellular and Molecular Mechanisms
McIntosh, T. K., Saatman, K. E., & Raghupathi, R. (1997) · The Neuroscientist · doi:10.1177/107385849700300310 · Cited by 45
Self-citationPKC activator therapeutic for mild traumatic brain injury in mice
Zohar, O., Lavy, R., Zi, X., Nelson, T. J., Hongpaisan, J., Pick, C. G., & Alkon, D. L. (2010) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.10.001 · Cited by 53
“One of TBI's secondary consequences is increased synthesis and expression of the amyloid precursor protein (APP) and its proteolytic product βA, which is the main constituent of plaques observed in brains of Alzheimer's disease (AD) patients (Gorrie et al., 2002; Pierce et al., 1996; Lewen et al., 1995; Murai et al.,…”
BackgroundLopez Sanchez, M. I. G., Waugh, H. S., Tsatsanis, A., Wong, B. X., Crowston, J. G., Duce, J. A., & Trounce, I. A. (2017) · Scientific Reports · doi:10.1038/s41598-017-10233-0 · Cited by 45
Bird, S., Sohrabi, H. R., Sutton, T. A., Weinborn, M., Rainey‐Smith, S. R., Brown, B. M., Patterson, L. C., Taddei, K., Gupta, V. B., Carruthers, M. E., et al. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.01.004 · Cited by 46
Collins, J. M., King, A. E., Woodhouse, A., Kirkcaldie, M. T. K., & Vickers, J. C. (2015) · Experimental Neurology · doi:10.1016/j.expneurol.2015.02.034 · Cited by 43
“While most human TBI cases are not genetically predisposed to AD, such mutations are necessary in mice to produce Aβ plaques as Wt rodents do not form plaques with aging (Selkoe, 1989) or after TBI (Pierce et al., 1996; Bramlett et al., 1997; Murai et al., 1998).”
Acute Blast Injury Reduces Brain Abeta in Two Rodent Species
Gasperi, R. D., Sosa, M. A. G., Kim, S. H., Steele, J., Shaughness, M., Maudlin-Jeronimo, E., Hall, A. A., DeKosky, S. T., McCarron, R. M., Nambiar, M. P., et al. (2012) · Frontiers in Neurology · doi:10.3389/fneur.2012.00177 · Cited by 45
“Amyloid precursor protein accumulation in axons is widely used as a marker of axonal injury in both humans and experimental animal models of nbTBI (Gentleman et al., 1993; Sherriff et al., 1994; Lewen et al., 1995; Pierce et al., 1996; Stone et al., 2000).”
BackgroundKoob, A. O., & Borgens, R. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20837 · Cited by 43
“APP also accumulates in injured axons after traumatic axonal injury (TAI) of the rat (Lewen et al., 1995; Pierce et al., 1996; Bramlett et al., 1997) and in various disease states of animals and man (Maccioni et al., 2001).”
BackgroundHuh, J. W., Franklin, M. A., Widing, A. G., & Raghupathi, R. (2006) · Developmental Neuroscience · doi:10.1159/000094172 · Cited by 40
Brodhun, M., Fritz, H., Walter, B. L., Antonow‐Schlorke, I., Reinhart, K., Zwiener, U., Bauer, R., & Patt, S. (2001) · Acta Neuropathologica · doi:10.1007/s004010000290 · Cited by 40
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van den Heuvel, C., Donkin, J., Finnie, J., Blumbergs, P., Kuchel, T., Koszyca, B., Manavis, J., Jones, N., Reilly, P., & Vink, R. (2004) · Journal of Neurotrauma · doi:10.1089/neu.2004.21.1562 · Cited by 39
“Recent studies examining APP expression following traumatic brain injury (TBI) have shown that the APP protein is increased after injury (Lewen et al., 1995, 1996; Pierce et al., 1996; Bramlett et al., 1997), possibly as an acute phase response to trauma.”
InfluentialMaldonado, T. A., Jones, R. E., & Norris, D. O. (2002) · Journal of Neurobiology · doi:10.1002/neu.10090 · Cited by 38
Targeting neurodegeneration to prevent post-traumatic epilepsy.
Ali, I., Silva, J. C., Liu, S., Shultz, S. R., Kwan, P., Jones, N. C., & O'Brien, T. J. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2018.08.006 · Cited by 38
Quantitative imaging of tyrosine hydroxylase and calmodulin in the human brain
Sutoo, D., Akiyama, K., & Yabe, K. (2001) · Journal of Neuroscience Research · doi:10.1002/1097-4547(20010301)63:5 · Cited by 17
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“Male Sprague-Dawley rats weighing 300-400 g used in this study were prepared for fluid-percussion brain injury as described by Pierce et al. (1996) with some modifications.”
InfluentialMolecular Mechanisms Underlying Effects of Neural Stem Cells against Traumatic Axonal Injury
Wang, E., Gao, J.-L., Yang, Q., Parsley, M. O., Dunn, T. J., Zhang, L., Dewitt, D., Denner, L., Prough, D., & Wu, P. (2012) · Journal of Neurotrauma · doi:10.1089/neu.2011.2043 · Cited by 34
“Furthermore, amyloid b -precur- sor protein (APP or b APP), a marker for abnormal axonal transport (Geddes et al., 2000; Gentleman et al., 1993; Mar-marou & Povlishock, 2006; Pierce et al., 1996; Stone et al., 2000), was increased by TBI.”
HOSHINO, S., Kobayashi, S., Furukawa, T., Asakura, T., & Teramoto, A. (2003) · Neurologia medico-chirurgica · doi:10.2176/nmc.43.165 · Cited by 35
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Animal Models of Traumatically-Induced Dementia
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Mechanical stress models of Alzheimer's disease pathology
Lévy, M., Epelbaum, S., Steyaert, J., Dubois, B., & Schwartz, L. H. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.10.005 · Cited by 37
“[88] Pierce JE, Trojanowski JQ, Graham DI, Smith DH, McIntosh TK.”
Okubo, S., Xi, G., Keep, R., Muraszko, K., & Hua, Y. (2013) · Acta neurochirurgica. Supplement · doi:10.1007/978-3-7091-1434-6_14 · Cited by 32
The Amyloid Precursor Protein Is a Conserved Receptor for Slit to Mediate Axon Guidance
Wang, B.-P., Li, H., Mutlu, S., Bowser, D., Moore, M., Wang, M. C., & Zheng, H. (2017) · eNeuro · doi:10.1523/eneuro.0185-17.2017 · Cited by 31
“However, under neuropathological conditions, such as traumatic brain injury (TBI) and AD, some of the developmental guidance processes may be re-activated.”
BackgroundImmunoreactivity of β-amyloid precursor protein in amyotrophic lateral sclerosis
Sasaki, S., & Iwata, M. (1999) · Acta Neuropathologica · doi:10.1007/s004010051015 · Cited by 31
Chang, P., Williams, A. M., Bhatti, U. F., Biesterveld, B. E., Liu, B., Nikolian, V. C., Dennahy, I. S., Lee, J., Li, Y., & Alam, H. B. (2019) · Journal of the American College of Surgeons · doi:10.1016/j.jamcollsurg.2018.12.026 · Cited by 36
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“The number of plaque-distant axonal swellings with a diameter of larger than 10 μm was quantified in the pons and spinal cord using antibodies towards pAPP (anti-pT668) and neurofilament (NF-200) as markers of axonopathy.”
MethodChanges in regional energy metabolism after closed head injury in the rat
Mautes, A., Thomé, D., Steudel, W., Nacimiento, A., Yang, Y., & Shohami, E. (2001) · Journal of Molecular Neuroscience · doi:10.1385/jmn:16:1:33 · Cited by 29
“Therefore, the present study was designed to evaluate the temporal changes in ATP, glucose, and lactate levels at various intervals after CHI, in an attempt to correlate these changes with the changes in inflammatory mediators, which are major components in the pathophysiology of TBI.”
BackgroundInfluentialShishido, 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
Profiling biomarkers of traumatic axonal injury: From mouse to man
Manivannan, S., Makwana, M., Ahmed, A. I., & Zaben, M. (2018) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2018.05.017 · Cited by 32
van den Heuvel, C., Blumbergs, P., Finnie, J. W., Manavis, J., Lewis, S., Jones, N. R., Reilly, P. L., & Pereira, R. A. (2000) · Journal of clinical neuroscience · doi:10.1054/jocn.1999.0168 · Cited by 28
Loring, J. F., Pászty, C., Rose, A., McIntosh, T. K., Murai, H., Pierce, J. E. S., Schramm, S. R., Wymore, K., Lee, V. M. ‐., Trojanowski, J. Q., et al. (1996) · Neurobiology of Aging · doi:10.1016/0197-4580(95)02076-4 · Cited by 29
Self-citationNew Method for the Quantitative Assessment of Axonal Damage in Focal Cerebral Ischemia
Imai, H., Mcculloch, J., Graham, D. I., Masayasu, H., & Macrae, I. M. (2002) · Journal of Cerebral Blood Flow and Metabolism · doi:10.1097/00004647-200209000-00005 · Cited by 27
“Accumulation of APP (in axonal tracts exhibiting morphologic abnormalities) has consequently been used to characterize axonal injury after head injury (Pierce et al., 1996; Bramlett et al., 1997; Gentleman et al., 1999; Graham et al., 2000) and ischemic injury (Yam et al.”
BackgroundMethodSelf-citationDoes human βA4 exert a protective function against oxidative stress in Alzheimer’s disease?
Berthon, G. (2000) · Medical Hypotheses · doi:10.1054/mehy.1999.0924 · Cited by 26
Xie, Y., Yao, Z., Chai, H., Wong, W., & Wu, W. (2003) · Journal of Neuroscience Research · doi:10.1002/jnr.10667 · Cited by 21
“Experimental ischemia (Wakita et al., 1992; Kalaria et al., 1993; Pierce et al., 1996) and injection of excitotoxic compounds (Siman et al.”
BackgroundZanello, S. B., Theriot, C. A., Ponce, C. M. P., & Chévez‐Barrios, P. (2013) · Gravitational and Space Research · doi:10.2478/gsr-2013-0003 · Cited by 27
“…rats, and pigs (Smith et al., 1999), by tracing not only the full-length protein but also small aminoacid peptides. β-amyloid was present in areas of the brain as soon as one day after brain trauma was provoked by pressure injection of saline into the cranium in a rat model (Pierce et al., 1996).”
BackgroundTraumatic brain injury recapitulates developmental changes of axons
Song, H., Chen, C., Kelley, B. J., Tomasevich, A., Lee, H., Dollé, J.-P., Cheng, J., Garcia, B. A., Meaney, D. F., & Smith, D. H. (2022) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2022.102332 · Cited by 25
“The rats were sacrificed at 24 h after lateral FPI, when extensive axonal injuries were expected (Koch et al., 2020; Pierce et al., 1996).”
Self-citationLippert-Gruener, M., Maegele, M., Garbe, J., & Angelov, D. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2006.07.025 · Cited by 24
Li, Y., Zhang, L., Kallakuri, S., Cohen, A., & Cavanaugh, J. M. (2015) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2015.08.035 · Cited by 26
Reduction of pTau and APP levels in mammalian brain after low-dose radiation
Iacono, D., Murphy, E. K., Avantsa, S. S., Perl, D. P., & Day, R. M. (2021) · Scientific Reports · doi:10.1038/s41598-021-81602-z · Cited by 19
Portbury, S. D., & Adlard, P. A. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-143048 · Cited by 26
“Non-transgenic rat TBI models reproduced intra-axonal A PP accumulation, but no associated A accumulation in axons or plaques [63, 64].”
Galvin, J. E., Nakamura, M., McIntosh, T. K., Saatman, K. E., Sampathu, D. M., Raghupathi, R., Lee, V. M. ‐., & Trojanowski, J. Q. (2000) · Experimental Neurology · doi:10.1006/exnr.2000.7461 · Cited by 20
Self-citationPosttraumatic epilepsy induced by lateral fluid-percussion brain injury in rats
Pitkänen, A., Kharatishvili, I., Nissinen, J., & McIntosh, T. (2006) · Elsevier eBooks · doi:10.1016/b978-012088554-1/50039-6 · Cited by 20
Self-citationMcCunn, P., Xu, X., Moszczynski, A. J., Li, A., Brown, A. M., & Bartha, R. (2021) · Journal of Neuroimaging · doi:10.1111/jon.12917 · Cited by 18
Mai, W.-H., Hu, X.-Q., Lu, Z.-H., Peng, F.-H., & Wang, Y.-G. (2011) · Journal of International Medical Research · doi:10.1177/147323001103900641 · Cited by 17
Itoh, T., Satou, T., Nishida, S., Tsubaki, M., Hashimoto, S., & Ito, H. (2009) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-008-0013-1 · Cited by 17
“APP is upregulated acutely in injured neurons and reactive astrocytes following TBI [26, 27], and this upregulation has been associated with increase hippocampal cell death [6].”
BackgroundSynuclein aggregation: possible role in traumatic brain injury
Bramlett, H. M., & Dietrich, W. D. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00401-1 · Cited by 17
van den Heuvel, C., Finnie, J., Blumbergs, P., Manavis, J., Jones, N., Reilly, P., & Pereira, R. A. (2000) · Journal of Neurotrauma · doi:10.1089/neu.2000.17.1041 · Cited by 16
“…1993; McKenzie et al., 1994; Roberts et al., 1994) and in various experimental models of TBI (Kawarabayashi et al., 1991; Nakamura et al., 1992; Shigematsu and McGeer, 1992a, 1992b; Hajimohammadreza et al., 1994; Lewen et al., 1996; Pierce et al., 1996; Bramlett et al., 1997; Lin et al., 1998).”
Pernici, C. D., Rowe, R. K., Doughty, P. T., Madadi, M., Lifshitz, J., & Murray, T. A. (2020) · Scientific Reports · doi:10.1038/s41598-020-64783-x · Cited by 17
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
“APP mRNA and protein expression is upregulated acutely after experimental TBI (Ciallella et al., 2002; Murakami et al., 1998; Pierce et al., 1996), resulting in axonal accumulation of APP (Gentleman et al.”
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
Rajendran, R., Rajendran, V., Giraldo‐Velásquez, M., Megalofonou, F.-F., Gurski, F., Stadelmann, C., Karnati, S., & Berghoff, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22179495 · Cited by 14
“APP is a well-characterized marker to detect axonal injury in neurodegenerative diseases such as MS [51,52].”
BackgroundExplosive-driven double-blast exposure: molecular, histopathological, and behavioral consequences
Murphy, E. K., Iacono, D., Pan, H., Grimes, J., Parks, S., Raiciulescu, S., Leonessa, F., & Perl, D. (2020) · Scientific Reports · doi:10.1038/s41598-020-74296-2 · Cited by 14
Singh, A. (2017) · Brain Injury · doi:10.1080/02699052.2017.1321781 · Cited by 14
“β APP, a normal constituent of neurons, is transported by the fast mode of anterograde axoplasmic transport and rapidly pools at sites of focally impaired transport [22,34–46], thereby serving as a useful early marker of TBI (within 3-hour survival post-TBI) [22,41,45].”
BackgroundClearance of Amyloid-β Protein Deposits in Transgenic Mice following Focal Cerebral Ischemia
Nostrand, W. E. V., Davis, J., Previti, M. L., & Xu, F. (2012) · Neurodegenerative Diseases · doi:10.1159/000334763 · Cited by 15
Inampudi, C., Ciccotosto, G. D., Cappai, R., & Crack, P. J. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6955 · Cited by 12
Leclercq, P., Stephenson, M. S., Murray, L. S., McIntosh, T., Graham, D., & Gentleman, S. (2002) · Journal of Neurotrauma · doi:10.1089/08977150260337985 · Cited by 13
“A similar minimum delay can be seen in animal percussion models (Lewen et al., 1995; Pierce et al., 1996) and as early as 30 min in an impact acceleration model (Stone et al., 2000a).”
Self-citationProgress Toward a Multiomic Understanding of Traumatic Brain Injury: A Review
Kocheril, P. A., Moore, S. C., Lenz, K. D., Mukundan, H., & Lilley, L. M. (2022) · Biomarker Insights · doi:10.1177/11772719221105145 · Cited by 16
Blizzard, C. A., King, A. E., Vickers, J. C., & Dickson, T. C. (2013) · Journal of Neurotrauma · doi:10.1089/neu.2013.2850 · Cited by 14
1. Traumatic brain injury: Prevention, pathophysiology, and outcome prediction
Sandel, M., Bell, K. R., & Michaud, L. (1998) · Archives of Physical Medicine and Rehabilitation · doi:10.1016/s0003-9993(98)90113-7 · Cited by 12
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
“Using the lateral fluid percussion (LFP) model in rats (McIntosh and Vink 1989, Dietrich et al. 1996, Pierce and Trojanowski 1996), numerous investigations describe the major histopathological consequences to trauma: lesion-induced vascular perturbations (Cortez and McIntosh 1989, Schmidt and Grady…”
BackgroundResultInfluentialSimpkins, J. W., Gatson, J. W., & Wigginton, J. G. (2009) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2009.01.013 · Cited by 5
“[11] Pierce JE, Trojanowski JQ, Graham DI, Smith DH, McIntosh TK.”
BackgroundEzra, Y., Oron, L., Moskovich, L., Roses, A. D., Beni, S. M., Shohami, E., & Michaelson, D. M. (2003) · Neuroscience · doi:10.1016/s0306-4522(03)00436-6 · Cited by 11
“Previous experiments revealed that the rat brain APP and APPs levels are significantly increased following head trauma (Lewen et al., 1996; Pierce et al., 1996).”
BackgroundChuang, J., & Chen, S. T. (2002) · Neurochemistry International · doi:10.1016/s0197-0186(01)00075-4 · Cited by 11
Exposure to Low-Intensity Blast Increases Clearance of Brain Amyloid Beta
Abutarboush, R., Reed, E., Chen, Y., Gu, M., Watson, C., Kawoos, U., Statz, J. K., Tschiffely, A. E., Ciarlone, S. L., Garcia, G. S. P., et al. (2024) · Journal of Neurotrauma · doi:10.1089/neu.2023.0284 · Cited by 9
“11,67,68 APP levels did not change in Triton-fractions 1d post-blast; however, reduction in Triton APP was observed 28d post-blast and did not correspond with A b levels at 28d. Similarly, APP reduction in PBS-fractions did not correspond with the observed changes in PBS or Triton-soluble A b pools…”
Traumatic MicroRNAs: Deconvolving the Signal After Severe Traumatic Brain Injury
Cente, M., Matyasova, K., Csicsatkova, N., Tomikova, A., Porubska, S., Niu, Y., Majdan, M., Filipcik, P., & Jurisica, I. (2022) · Cellular and molecular neurobiology · doi:10.1007/s10571-022-01254-z · Cited by 9
“The accumulation of APP was observed already after 1 h following the diffuse axonal injury and persisted for 2 weeks in a specific brain region of rat TBI model (Pierce et al. 1996).”
BackgroundDating of Traumatic Brain Injury in Forensic Cases Using Immunohistochemical Markers (I)
Tirado, M. D. L. Á. R., Pampín, J. B., & Gomez, R. G. (2018) · American Journal of Forensic Medicine & Pathology · doi:10.1097/paf.0000000000000412 · Cited by 13
MCP-1-Induced Migration of NT2 Neuroprogenitor Cells Involving APP Signaling
Vrotsos, E., & Sugaya, K. (2009) · Cellular and molecular neurobiology · doi:10.1007/s10571-008-9329-3 · Cited by 8
“Other studies report that traumatic brain injury can induce expression of APP (Pierce et al. 1996; Murakami et al. 1998; Ciallella et al. 2002).”
BackgroundConnecting cellular mechanisms and extracellular vesicle cargo in traumatic brain injury
Ollen‐Bittle, N., Roseborough, A. D., Wang, W., Wu, J.-L. D., & Whitehead, S. N. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.391329 · Cited by 9
“In keeping with Winston and colleagues findings of increased Aβ in neuronal and astrocytic derived EVs post TBI, studies in rats have similarly shown an increase in APP in both neurons and astrocytes post TBI (JE Pierce et al., 1996; Bramlett et al., 1997).”
BackgroundHetzer, S., O'Connell, C., Lallo, V., Robson, M., & Evanson, N. (2023) · bioRxiv · doi:10.1101/2023.05.25.542261 · Cited by 7
“APP staining has long been employed as a measure for detecting axonal injury after TBI (Blumbergs et al., 1995; Bramlett et al., 1997; Gentleman et al., 1993; Pierce et al., 1996).”
MethodPathological Links between Traumatic Brain Injury and Dementia: Australian Pre-Clinical Research
Collins, J. M., Woodhouse, A., Bye, N., Vickers, J. C., King, A. E., & Ziebell, J. M. (2020) · Journal of Neurotrauma · doi:10.1089/neu.2019.6906 · Cited by 8
“27 However, Australian neurotrauma researchers 89,97 and others 26,87,88 have also demonstrated an increase in neuronal APP staining after TBI.”
Neuropathology of Traumatic Brain Injury and Its Role in the Development of Alzheimer’s Disease
Villapol, S. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.81945 · Cited by 5
Schulze, P., Thal, D., Bettag, M., & Schober, R. (1998) · doi:10.1111/j.1440-1789.1998.tb00078.x · Cited by 5
Tran, H. (2011) · Open Scholarship Institutional Repository (Washington University in St. Louis) · doi:10.7936/k7gb223z
Junyent, F., Utrera, J., & Auladell, C. (2006) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2006.05199.x · Cited by 4
“Moreover, axonal APP accumulation, noticeably observed at P15 in treated animals, supports the notion of axonal damage (Pierce et al., 1996; Stone et al., 1999; Chen et al., 2004).”
BackgroundTruong, P. H., Crouch, P. J., Hilton, J. B. W., McLean, C., Cappai, R., & Ciccotosto, G. D. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03924-5 · Cited by 3
The Amyloid Precursor-like Protein APL-1 Regulates Axon RegenerationPreprint
Zeng, L., Bejjani, R. M. E., & Hammarlund, M. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/305284 · Cited by 3
“Similar accumulation of APP has been observed in injured mammalian neurons (Gentleman et al., 1993; Otsuka et al., 1991; Pierce et al., 1996); in fact, APP has often been used as a marker for axonal injury (summarized in Stone et al., 2000).”
Background
Metadata
- Authors
- Pierce, J., Trojanowski, J., Graham, D., Smith, D., & McIntosh, T.
- Affiliations
- University of Pennsylvania (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1996-02-01
- Volume
- 16
- Issue
- 3
- Pages
- 1083-1090
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6578806
- OpenAlex
- W1879457624
- Cited by
- 239
- References
- 75
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 8 · 2018: 7 · 2017: 8 · 2016: 5 · 2015: 15 · 2014: 4 · 2013: 10 · 2012: 8
- FWCI
- 10.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (P30AG010124, AG-10124)
- National Institute of Neurological Disorders and Stroke (NS-08803, NS26818)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- amyloid precursor protein, amyloid-beta, traumatic brain injury, fluid percussion injury, axonal pathology, neurodegeneration, thalamus, white matter, hippocampus, striatum
- MeSH terms
- Animals, Brain Injuries, Hippocampus, Male, Nerve Degeneration, Nerve Tissue Proteins, Pressure, Thalamus, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Rats, Sprague-Dawley, Rats
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