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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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.
“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]
The Discussion (page not available in our copy) reports increased APP/APLP immunoreactivity in the thalamus at 1 hour and in the striatum, hippocampus, and injured cortex by 2 hours after lateral fluid-percussion injury. This paper does not study impact injury, and the Results place increased staining in cortical and thalamic neuronal cell bodies at 48 hours or later, not within the first 24 hours. It measures APP/APLP accumulation and immunoreactivity rather than establishing increased APP expression. (LLM, conf=0.88)
Experimental — accuracy not yet measuredA majority of rodent studies fail to show Aβ deposition after TBI in non-transgenic animals using CCI, FPI, and weight drop models.
“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]
The Discussion (page unavailable) reports no Aβ deposits after lateral fluid-percussion injury in rats and describes a weight-drop study with no evidence of Aβ deposits. It does not address CCI or establish that a majority of rodent studies found no deposition. (LLM, conf=0.84)
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ResultAlzheimer Disease and Its Growing Epidemic
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BackgroundSmith, D. H., Nakamura, M., McIntosh, T. K., Wang, J., Rodríguez, A., Chen, X.-H., Raghupathi, R., Saatman, K. E., Clemens, J., Schmidt, M. L., et al. (1998) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)65643-x · Cited by 143 · see citing works
Self-citationAlbayram, Ö., Kondo, A., Mannix, R., Smith, C., Tsai, C.-Y., Li, C., Herbert, M. K., Qiu, J., Monuteaux, M. C., Driver, J. A., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-01068-4 · Cited by 152 · see citing works
“The primary antibodies used were cis mAb (clone #113) and trans mAb (clone #25)48, tau tangle-related mAbs AT180, AT8, AT100 (all from Innogenetics, Alpharetta, GA), oligomeric tau T22 polyclonal antibodies (EMD Millipore, Billerica, MA), anti-tau rabbit mAb (E178, Abcam), anti-PHF-1 (ab109390, Abcam), Von Willerbrand…”
BackgroundFlygt, J., Djupsjö, A., Lenne, F., & Marklund, N. (2013) · European Journal of Neuroscience · doi:10.1111/ejn.12179 · Cited by 144 · see citing works
“…et al. (2011a,b); similar IHC staining pattern APP Anti-rabbit Amyloid precursor protein 51 2700: Invitrogen Coporation, Camarillo, CA, USA WB Pierce et al. (1996), Wang et al. (2011); similar IHC staining pattern CC1 Anti-mouse Mature OLs ab16794: Abcam, Cambridge, UK ICC,…”
Spain, 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 133 · see citing works
“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).”
Aβ as a bioflocculant: implications for the amyloid hypothesis of Alzheimer’s disease
Robinson, S. R., & Bishop, G. M. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(01)00342-6 · Cited by 153 · see citing works
van den Heuvel, C., Blumbergs, P. C., Finnie, J. W., Manavis, J., Jones, N. R., Reilly, P. L., & Pereira, R. A. (1999) · Experimental Neurology · doi:10.1006/exnr.1999.7150 · Cited by 130 · see citing works
Marklund, N., Blennow, K., Zetterberg, H., Ronne-Engström, E., Enblad, P., & Hillered, L. (2009) · Journal of Neurosurgery · doi:10.3171/2008.9.jns08584 · Cited by 135 · see citing works
Metz, I., Lucchinetti, C., Openshaw, H., García-Merino, A., Lassmann, H., Freedman, M., Atkins, H., Azzarelli, B., Kolar, O., & Brück, W. (2007) · Brain : a journal of neurology · doi:10.1093/brain/awl370 · Cited by 135 · see citing works
Stone, J. R., Singleton, R. H., & Povlishock, J. T. (2000) · Brain Research · doi:10.1016/s0006-8993(00)02485-9 · Cited by 132 · see citing works
Apolipoprotein E &egr;4 and short-term recovery from predominantly mild brain injury
Liberman, J., Stewart, W., Wesnes, K., & Troncoso, J. (2002) · Neurology · doi:10.1212/wnl.58.7.1038 · Cited by 129 · see citing works
The 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 · see citing works
“Although Aβ deposition is apparent following rotational acceleration TBI in pigs (132, 133) and rabbits (134), 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).”
BackgroundHerrero-Herranz, E., Pardo, L., Gold, R., & Linker, R. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.01.001 · Cited by 124 · see citing works
“APP is a well characterized marker for acute axonal injury in neurodegenerative diseases, but also MS (Kuhlmann et al., 2002; Pierce et al., 1996).”
BackgroundIwata, 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 · see citing works
Self-citationNitric oxide generators produce accumulation of chelatable zinc in hippocampal neuronal perikarya
Cuajungco, M. P., & Lees, G. J. (1998) · Brain Research · doi:10.1016/s0006-8993(98)00463-6 · Cited by 115 · see citing works
Traumatic brain injury: cause or risk of Alzheimer’s disease? A review of experimental studies
Szczygielski, J., Mautes, A. E. M., Steudel, W. I., Falkai, P., Bayer, T. A., & Wirths, O. (2005) · Journal of Neural Transmission · doi:10.1007/s00702-005-0326-0 · Cited by 75 · see citing works
“Nevertheless, APP immunostaining remains to be so far the best method to visualise injured axons, both in experimental (Bramlett et al., 1997; Pierce et al., 1996; Stone et al., 1999; Hoshino et al., 2003) and medical settings (Gentleman et al., 1993b; Sherriff et al., 1994a, b; Blumbergs et al.,…”
BackgroundMethodInfluentialLifshitz, J., Kelley, B., & Povlishock, J. (2007) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/01.jnen.0000248558.75950.4d · Cited by 114 · see citing works
“To date, the long-term fate of neurons subjected to perisomatic axotomy has not been followed over a prolonged time course because of the persistent evolution of the injury cavity after focal injuries and the resorption of axonal pathology after diffuse injury (3, 6).”
BackgroundAnimal Models of Post-Traumatic Epilepsy
Pitkänen, A., & McIntosh, T. (2006) · Journal of Neurotrauma · doi:10.1089/neu.2006.23.241 · Cited by 112 · see citing works
“…that axonal injury continues for weeks to months post-injury in the major fiber pathways in mice, rats, and humans, and therefore, occurs in parallel with axonal sprouting (Roberts et al., 1991; Graham et al., 1995; Pierce et al., 1996; Carbonnell and Grady, 1999; Bramlett and Dietrich, 2002).”
Self-citationRodent Model of Direct Cranial Blast Injury
Kuehn, R. B., Simard, P. F., Driscoll, I., Keledjian, K., Ivanova, S. A., Tosun, Ç., Williams, A. N., Bochicchio, G., Gerzanich, V., & Simard, J. M. (2011) · Journal of Neurotrauma · doi:10.1089/neu.2010.1532 · Cited by 109
“Both axonal and neuronal abnormalities were identified that were broadly similar to findings reported in other forms of TBI (Blumbergs et al., 1995; Bramlett et al., 1997; Itoh et al., 2009; Kilbourne et al., 2009; Pierce et al., 1996; Stone et al., 2000).”
Brain 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 104 · see citing works
“…models have relatively low abundance of brain endogenous Aβ species that do not reach a critical threshold for aggregation (Lewen et al., 1995; Pierce et al., 1996; Bramlett et al., 1997; Hoshino et al., 1998; Iwata et al., 2002; Stone et al., 2002; Hamberger et al., 2003; Abrahamson et al.,…”
BackgroundEffects of Low-Level Blast Exposure on the Nervous System: Is There Really a Controversy?
Elder, G. A., Stone, J. R., & Ahlers, S. T. (2014) · Frontiers in Neurology · doi:10.3389/fneur.2014.00269 · Cited by 109 · see citing works
Tsitsopoulos, P. P., & Marklund, N. (2013) · Frontiers in Neurology · doi:10.3389/fneur.2013.00079 · Cited by 114 · see citing works
“In addition, increased neuronal APP expression has also been observed in human and animal models and across the spectrum of severe TBI (Otsuka et al., 1991; Sola et al., 1993; Lewen et al., 1995; Pierce et al., 1996; Murakami et al., 1998; Ciallella et al., 2002; Itoh et al., 2009).”
BackgroundInfluentialNovel Model of Frontal Impact Closed Head Injury in the Rat
Kilbourne, M., Kuehn, R. B., Tosun, Ç., Caridi, J., Keledjian, K., Bochicchio, G., Scalea, T., Gerzanich, V., & Simard, J. M. (2009) · Journal of Neurotrauma · doi:10.1089/neu.2009.0968 · Cited by 107 · see citing works
“Diffuse axonal injury (DAI) is characterized by the accumulation of b-APP in injured axons in a pattern that resembles a string of beads (Blumbergs et al., 1995; Bramlett et al., 1997; Pierce et al., 1996; Stone et al., 2000).”
Mechanisms of amyloid plaque pathogenesis
Fiala, J. C. (2007) · Acta Neuropathologica · doi:10.1007/s00401-007-0284-8 · Cited by 98 · see citing works
Washington, P. M., Morffy, N., Parsadanian, M., Zapple, D. N., & Burns, M. P. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3017 · Cited by 103 · see citing works
Rodriguez-Paez, A. C., Brunschwig, J. P., & Bramlett, H. M. (2005) · Acta Neuropathologica · doi:10.1007/s00401-005-1010-z · Cited by 94 · see citing works
“b-Amyloid precursor protein (bAPP), an effective marker for axonal damage [10, 31, 34, 44, 69, 76], is transported by fast axoplasmic flow and accumulates following cytoskeletal disruption [58].”
Sanderson, K. L., Raghupathi, R., Saatman, K., Martin, D., Miller, G., & McIntosh, T. (1999) · Journal of Cerebral Blood Flow and Metabolism · doi:10.1097/00004647-199910000-00008 · Cited by 98 · see citing works
Self-citationThe Neuroprotective Properties of the Amyloid Precursor Protein Following Traumatic Brain Injury
Plummer, S. L., van den Heuvel, C., Thornton, E., Corrigan, F., & Cappai, R. (2016) · Aging and Disease · doi:10.14336/ad.2015.0907 · Cited by 103 · see citing works
“The amyloid precursor protein (APP) has a long association with TBI as its expression is dramatically upregulated in the brain following injury [3-6].”
BackgroundResultInfluentialGenetic vulnerability following traumatic brain injury: the role of apolipoprotein E
Nathoo, N. (2003) · Molecular Pathology · doi:10.1136/mp.56.3.132 · Cited by 96 · see citing works
Apoptotic and behavioral sequelae of mild brain trauma in mice
Tweedie, D., Milman, A., Holloway, H., Li, Y.-Z., Harvey, B., Shen, H., Pistell, P., Lahiri, D., Hoffer, B., Wang, Y., et al. (2007) · Journal of Neuroscience Research · doi:10.1002/jnr.21160 · Cited by 96 · see citing works
Stone, J., Walker, S. A., & Povlishock, J. (1999) · Acta Neuropathologica · doi:10.1007/s004010050996 · Cited by 95 · see citing works
Ciallella, J. R., Ikonomovic, M. D., Paljug, W. R., Wilbur, Y. I., Dixon, C. E., Kochanek, P. M., Marion, D. W., & DeKosky, S. T. (2002) · Journal of Neurotrauma · doi:10.1089/089771502762300229 · Cited by 94 · see citing works
“However, A b deposits were not detected at any time post-injury in any brain region examined, consistent with studies using fluid-per-cussion (Pierce et al., 1996; Masumura et al., 2000) or weight-drop (Lewen et al., 1996) models of brain Because we found no A b deposits in brain regions analyzed…”
InfluentialBehavioral 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).”
MethodMorrison, B., Eberwine, J., Meaney, D., & McIntosh, T. (2000) · Neuroscience · doi:10.1016/s0306-4522(99)00537-0 · Cited by 92 · see citing works
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 · see citing works
Self-citationAbrahamson, E. E., Ikonomovic, M. D., Ciallella, J. R., Hope, C. E., Paljug, W. R., Isanski, B. A., Flood, D. G., Clark, R. S. B., & DeKosky, S. T. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2005.10.011 · Cited by 90 · see citing works
APP as a Protective Factor in Acute Neuronal Insults
Hefter, D., & Draguhn, A. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00022 · Cited by 89 · see citing works
“…fluid percussion model of diffuse brain injury in adult rats APP expression was globally elevated in cortex and hippocampus within hours following the insult (Murakami et al., 1998); in a lateral fluid percussion model APP was overexpressed as early as 1 h after the insult (Pierce et al., 1996).”
BackgroundAnimal models of traumatic brain injury
Johnson, V. E., Meaney, D. F., Cullen, D. K., & Smith, D. H. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-52892-6.00008-8 · Cited by 146 · see citing works
“Similarly, neuronal loss and axonal pathology has been observed in regions distant to the contusion site (Dixon et al., 1991; Pierce et al., 1996).”
BackgroundSelf-citationVink, R., Mullins, P. G., Temple, M. D., Bao, W.-L., & Faden, A. (2001) · Journal of Neurotrauma · doi:10.1089/089771501316919201 · Cited by 87 · see citing works
“This observation of bilateral damage was supported in a later publication reporting that significant accumulations of amyloid precursor proteins occur in the ipsilateral hemisphere with changes some-times observed in the contralateral hemisphere as well (Pierce et al., 1996).”
Delayed Phospholipid Degradation in Rat Brain After Traumatic Brain Injury
Homayoun, P., de Turco, E., Parkins, N. E., Lane, D. C., Soblosky, J., Carey, M. E., & Bazan, N. (1997) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1997.69010199.x · Cited by 85 · see citing works
Povlishock, J., Buki, A., Koiziumi, H., Stone, J., & Okonkwo, D. (1999) · Acta neurochirurgica. Supplement · doi:10.1007/978-3-7091-6391-7_3 · Cited by 84 · see citing works
Extracellular association of APP and tau fibrils induces intracellular aggregate formation of tau
Takahashi, M., Miyata, H., Kametani, F., Nonaka, T., Akiyama, H., Hisanaga, S., & Hasegawa, M. (2015) · Acta Neuropathologica · doi:10.1007/s00401-015-1415-2 · Cited by 90 · see citing works
“It is not yet clear whether or not there is any increase in the expression levels of APP in brains of patients with sporadic AD, but it has been reported that the APP expression is increased in brains of post-traumatic injury patients [13, 47, 48] and animal models [21, 30, 43, 45, 59].”
BackgroundSchouten, J. W., Fulp, C. T., Royo, N. C., Saatman, K. E., Watson, D. J., Snyder, E. Y., Trojanowski, J. Q., Prockop, D. J., Maas, A. I. R., & McIntosh, T. K. (2004) · Journal of Neurotrauma · doi:10.1089/neu.2004.21.1501 · Cited by 73 · see citing works
“Secondary or delayed axotomy has been shown as early as 2–3 h after injury in clinical (McKenzie et al., 1996) and experimental (Pierce et al., 1996; Bramlett and Dietrich, 2002) TBI using amyloid precursor protein (APP) accumulation as a measure of axonal transport dysfunction.”
Self-citationBidmon, H.-J., Kato, K., Schleicher, A., Witte, O. W., & Zilles, K. (1998) · Stroke · doi:10.1161/01.str.29.1.203 · Cited by 82 · see citing works
Injury cascades in TBI-related neurodegeneration
DeKosky, S. T., & Asken, B. M. (2017) · Brain Injury · doi:10.1080/02699052.2017.1312528 · Cited by 91 · see citing works
OLIGODENDROCYTE VULNERABILITY FOLLOWING TRAUMATIC BRAIN INJURY IN RATS
Lotocki, G., Vaccari, J. P. D. R., Alonso, O., Molano, J. S., Nixon, R., Safavi, P., Dietrich, W., & Bramlett, H. (2011) · Neuroscience Letters · doi:10.1016/j.neulet.2011.05.056 · Cited by 79 · see citing works
Association of Chronic Vascular Changes with Functional Outcome after Traumatic Brain Injury in Rats
Hayward, N., Immonen, R. J., Tuunanen, P. I., Ndode‐Ekane, X. E., Gröhn, O. H. J., & Pitkänen, A. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2010.1448 · Cited by 80 · see citing works
“…that axonal injury in the thalamus after LFP injury is associated with chronic APP accumulation, which can lead to enhanced amyloid beta levels in the absence of plaques, as well as expression of enzymes processing APP (Bramlett et al., 1997; Johnson et al., 2010; Pierce, Trojanowski, et al. 1996).”
Alsop, D., Murai, H., Detre, J., McIntosh, T. K., & Smith, D. H. (1996) · Journal of Neurotrauma · doi:10.1089/neu.1996.13.515 · Cited by 79 · see citing works
“Since the understanding of diffusion is in such a primitive state, it is premature to assert that diffusion changes directly reflect axonal or dendritic damage but the close correlation between the distribution of acute diffusion change and the distribution of early axonal and dendritic damage as measured with /3APP a…”
InfluentialSelf-citationGensel, J., Wang, Y., Guan, Z., Beckwith, K. A., Braun, K. J., Wei, P., McTigue, D., & Popovich, P. (2015) · Journal of Neuroscience · doi:10.1523/jneurosci.0337-15.2015 · Cited by 75 · see citing works
“-APP is a sensitive measure of axon injury (Pierce et al., 1996).”
BackgroundBidmon, H.-J., Jancsik, V, Schleicher, A., Hagemann, G., Witte, O. W., Woodhams, P., & Zilles, K. (1997) · Neuroscience · doi:10.1016/s0306-4522(97)00289-3 · Cited by 74 · see citing works
Raghupathi, R., & McIntosh, T. K. (1996) · Molecular Brain Research · doi:10.1016/0169-328x(95)00289-5 · Cited by 72 · see citing works
Self-citationBaker, A. J., Phan, N., Moulton, R. J., Fehlings, M. G., Yücel, Y., Zhao, M., Liu, E., & Tian, G.-F. (2002) · Journal of Neurotrauma · doi:10.1089/089771502753754064 · Cited by 73 · see citing works
“Advantages include the availability of immunohistochemical techniques (Stone et al., 2000; Pierce et al., 1996) and the rapid appearance of increased staining following injury (McKenzie et al., 1996; Graham et al., 1995).”
McDermott, K. L., Raghupathi, R., Fernandez, S. C., Saatman, K. E., Protter, A. A., Finklestein, S. P., Sinson, G. P., Smith, D. H., & McIntosh, T. K. (1997) · Journal of Neurotrauma · doi:10.1089/neu.1997.14.191 · Cited by 73 · see citing works
“Although we did not quantitatively assess the cell loss in the thalamus, previous studies have reported both acute and delayed degeneration of thalamic neurons following FP brain injury (Hicks et al., 1996; Pierce et al., 1996).”
Self-citationEkmark‐Lewén, S., Flygt, J., Kiwanuka, O., Meyerson, B. J., Lewén, A., Hillered, L., & Marklund, N. (2013) · Journal of Neuroinflammation · doi:10.1186/1742-2094-10-44 · Cited by 67 · see citing works
“Increased β-APP immunostaining in white matter tracts is a consistent feature of experimental TBI models including the Marmarou impact acceleration and lateral fluid percussion injury (lFPI) models in rats [53-55].”
BackgroundSchultz, V., van der Meer, F., Wrzos, C., Scheidt, U., Bahn, E., Stadelmann, C., Brück, W., & Junker, A. (2017) · Glia · doi:10.1002/glia.23167 · Cited by 72 · see citing works
Harkany, T., Dijkstra, I., Oosterink, B. J., Horváth, K. M., Ábrahám, I., Keijser, J., van der Zee, E. A., & Luiten, P. (2000) · Neuroscience · doi:10.1016/s0306-4522(00)00296-7 · Cited by 68 · see citing works
Elder, G. A., Ehrlich, M. E., & Gandy, S. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.134294 · Cited by 73 · see citing works
Amyloid precursor protein potentiates the neurotrophic activity of NGF.
Wallace, W. C., Akar, C. A., & Lyons, W. E. (1997) · Brain Research. Molecular Brain Research · doi:10.1016/s0169-328x(97)00258-1 · Cited by 66 · see citing works
Lenzlinger, P. M., Shimizu, S., Marklund, N., Thompson, H. J., Schwab, M., Saatman, K., Hoover, R., Bareyre, F., Motta, M., Luginbuhl, A., et al. (2005) · Neuroscience · doi:10.1016/j.neuroscience.2005.04.048 · Cited by 65 · see citing works
Self-citationHamberger, A., Huang, Y.-L., Zhu, H., Bao, F., Ding, M., Blennow, K., Olsson, A., Hansson, H.-A., Viano, D., & Haglid, K. G. (2003) · Journal of Neurotrauma · doi:10.1089/08977150360547080 · Cited by 64 · see citing works
“It has been suggested that species differences in the processing of b APP and A b , and the characteristics of the antibodies used, are responsible for such discrepancies (Pierce et al., 1996; Smith et al., 1999).”
In Vivo Regulation of Amyloid Precursor Protein Secretion in Rat Neocortex by Cholinergic Activity
Roßner, S., Ueberham, U., Yu, J., Kirazov, L., Schliebs, R., Perez-Polo, J. R., & Bigl, V. (1997) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.1997.tb01379.x · Cited by 61 · see citing works
Decourt, B., D’Souza, G. X., Shi, J., Ritter, A., Suazo, J., & Sabbagh, M. N. (2022) · Aging and disease · doi:10.14336/ad.2021.0529 · Cited by 69 · see citing works
“Interestingly, astrocytes and microglia can also produce high amounts of Aβ during CNS insults [25].”
BackgroundSaatman, K., Zhang, C., Bartus, R., & Mcintosh, T. K. (2000) · Journal of Cerebral Blood Flow and Metabolism · doi:10.1097/00004647-200001000-00010 · Cited by 62 · see citing works
Self-citationHiltunen, M. O., van Groen, T., & Jolkkonen, J. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1154 · Cited by 56 · see citing works
“Brain insults, such as stroke and trauma, lead to a variable upregulation and accumulation of A β PP/ A β [2,3].”
Influential
- 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 › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › 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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