Brain Trauma Induces Massive Hippocampal Neuron Death Linked to a Surge in β-Amyloid Levels in Mice Overexpressing Mutant Amyloid Precursor Protein
Open accessAbstract
Although brain trauma is a risk factor for Alzheimer's disease, no experimental model has been generated to explore this relationship. We developed a model of brain trauma in transgenic mice that overexpress mutant human amyloid precursor protein (PDAPP) leading to the appearance of Alzheimer's disease-like beta-amyloid (Abeta) plaques beginning at 6 months of age. We induced cortical impact brain injury in the PDAPP animals and their wild-type littermates at 4 months of age, ie, before Abeta plaque formation, and evaluated changes in posttraumatic memory function, histopathology, and regional tissue levels of the Abeta peptides Abeta1-40 and Abeta1-42. We found that noninjured PDAPP mice had impaired memory function compared to noninjured wild-type littermates (P < 0.01) and that brain-injured PDAPP mice had more profound memory dysfunction than brain-injured wild-type littermates (P < 0.001). Although no augmentation of Abeta plaque formation was observed in brain-injured PDAPP mice, a substantial exacerbation of neuron death was found in the hippocampus (P < 0.001) in association with an acute threefold increase in Abeta1-40 and sevenfold increase in Abeta1-42 levels selectively in the hippocampus (P < 0.01). These data suggest a mechanistic link between brain trauma and Abeta levels and the death of neurons.
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CCI TBI induced a surge of plaque pathology in PDAPP mice soon after injury at 6 months of age, but a substantial reduction in cortical and hippocampal plaque load was detected chronically.
“Although CCI TBI induced a surge of plaque pathology in PDAPP mice soon after injury at 6 months of age, a substantial reduction in cortical and hippocampal plaque load was detected chronically (28, 40).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [28]
The Brain Injury section says the PDAPP mice were injured at 4 months of age, not 6 months. The Histopathological Analysis section reports no discernible difference in plaque number or distribution between injured and sham mice two months later, contradicting both the claimed surge in plaques and the claimed chronic reduction. The reported acute surge was in Aβ peptide levels, not plaque pathology (Aβ Tissue Levels section); page numbers are unavailable in our copy. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredMany animal studies show increased production and accumulation of amyloid precursor protein (APP), Aβ, and pathological tau following TBI.
“Second, many animal studies show increased production and accumulation of amyloid precursor protein (APP), Aβ, and pathological tau following TBI (16, 21–28).”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [28]
The Aβ Tissue Levels section reports an acute rise in Aβ after injury in PDAPP mice, and the introductory passage reports APP accumulation after trauma in experimental animals. The paper does not report pathological tau in injured animals; it mentions neurofibrillary tangles in human boxers. The Histopathological Analysis section also finds no increase in Aβ plaque deposition after injury, so the claim's accumulation language does not hold for plaques in this study. Page numbers are unavailable in our copy. (LLM, conf=0.88)
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“Many later studies reported lower memory scores in mice with CCI-induced brain injury compared to sham controls (Murai et al., 1998; Nakamura et al., 1999; Saatman et al., 2006; Schoch et al., 2012; Smith et al., 1998; Smith et al., 1995; Tomasevic et al., 2012; Zanier et al., 2011), and the memory score can also disc…”
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
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 CCI TBI induced a surge of plaque pathology in PDAPP mice soon after injury at 6 months of age, a substantial reduction in cortical and hippocampal plaque load was detected chronically (28, 40).”
BackgroundOlsson, A., Csajbok, L. Z., �st, M., H�glund, K., Nyl�n, K., Rosengren, L., Nellg�rd, B., & Blennow, K. (2004) · Journal of Neurology · doi:10.1007/s00415-004-0451-y · Cited by 138 · see citing works
“Firstly, Aβ deposition following head trauma has been observed in both man [8, 12, 31] and in experimental animal models [10, 36, 41].”
BackgroundInfluentialFee, D. B., Crumbaugh, A., Jacques, T. J., Herdrich, B. H., Sewell, D. L., Auerbach, D., Piaskowski, S. M., Hart, M., Sandor, M., & Fabry, Z. (2003) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(03)00008-0 · Cited by 127 · see citing works
“With the subsequent release of chemical factors and cytotoxins, a second period of destruction is entered, including oxidative stress, inflammation and apoptosis (Morrison et al., 1998; Raghupathi et al., 1998; Smith et al., 1998).”
BackgroundExperimental models of brain trauma
Laurer, H. L., & McIntosh, T. K. (1999) · Current Opinion in Neurology · doi:10.1097/00019052-199912000-00010 · Cited by 120 · see citing works
Self-citationIwata, A., Chen, X., McIntosh, T. K., Browne, K. D., & Smith, D. H. (2002) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/61.12.1056 · Cited by 116 · see citing works
“These findings are potentially in contrast with studies of transgenic mice, where only overexpression of KPI(1) APP mRNA has been shown to induce persistent Ab production (40, 62, 63).”
BackgroundResultSelf-citationThe Pathophysiology of Concussions in Youth
Shrey, D. W., Griesbach, G. S., & Giza, C. C. (2011) · Physical Medicine and Rehabilitation Clinics of North America · doi:10.1016/j.pmr.2011.08.002 · Cited by 110 · see citing works
“The injured hippocampi showed substantial exacerbation of neuronal death, which suggests that there is a mechanistic link between brain trauma, Ab levels, and neuronal cell death.(190) With repetitive mild TBI in Tg”
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
“This neuronal loss was accompanied by memory impairment, detected by the Morris Water Maze paradigm (Smith et al., 1998).”
BackgroundMethodHartman, R. E., Laurer, H., Longhi, L., Bales, K. R., Paul, S. M., McIntosh, T. K., & Holtzman, D. M. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-23-10083.2002 · Cited by 115 · see citing works
“Smith et al. (1998) reported that TBI in PDAPP mice resulted in an 84% loss of CA3 neurons compared with only a 36% loss in non-TG mice.”
Self-citationAcosta, S., Tajiri, N., Shinozuka, K., Ishikawa, H., Sanberg, P., Sánchez-Ramos, J., Song, S.-J., Kaneko, Y., & Borlongan, C. (2014) · PLoS ONE · doi:10.1371/journal.pone.0090953 · Cited by 115 · see citing works
“death, learning and memory impairments, aphasia, anxiety, and dementia are the most prevalent [12,13,14,15,16].”
BackgroundBrain 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
Yu, F., Zhang, Y., & Chuang, D. (2012) · Journal of Neurotrauma · doi:10.1089/neu.2012.2449 · Cited by 103 · see citing works
“Lithium treatment increases hippocampal preservation after TBI TBI-induced increases in Ab levels are known to correlate with massive neuronal death in the mouse hippocampus (Smith et al., 1998).”
BackgroundInfluentialEffects 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
“Interestingly, it has been shown that acute Aβ accumulations can be reversed following TBI (Smith et al., 1998).”
BackgroundResultThe role of innate immunity in Alzheimer's disease
Ennerfelt, H. E., & Lukens, J. R. (2020) · Immunological Reviews · doi:10.1111/imr.12896 · Cited by 121 · see citing works
The role of complement in Alzheimer’s disease pathology
Emmerling, M. R., Watson, M. D., Raby, C. A., & Spiegel, K. (2000) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/s0925-4439(00)00042-9 · Cited by 108 · see citing works
Emmerling, M., Morganti-Kossmann, M., Kossmann, T., Stahel, P. F., Watson, M. D., Evans, L., Mehta, P., Spiegel, K., Kuo, Y.-M., Roher, A., et al. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06357.x · Cited by 104 · see citing works
“With regard to Aβ1–42, the amount in CSF from TBI patients was significantly higher than that measured in CSF from control and AD subjects.6 Correlations between Aβ1–42 with ApoE (p 0.0001), tau (p 0.0001), or NSE (p 0.0001) have had similar and statistically significant “r values” (0.48–0.51), each accounting for abo…”
BackgroundInfluentialWashington, 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
The 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
Genetic 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
Alosco, M. L., Tripodis, Y., Fritts, N. G., Heslegrave, A., Baugh, C. M., Conneely, S. E., Mariani, M. L., Martin, B. M., Frank, S., Mez, J., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.05.004 · Cited by 121 · see citing works
Self-citationCiallella, 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
“In addition, one of these studies showed both greater memory deficits and hippocampal cell death after injury in transgenic mice compared to wild-type (Smith et al., 1998).”
Behavioral consequences of minimal traumatic brain injury in mice.
Zohar, O., Rubovitch, V., Milman, A., Schreiber, S., & Pick, C. G. (2011) · Acta Neurobiologiae Experimentalis · doi:10.55782/ane-2011-1821 · Cited by 93
“Since immobility was suggested to reflect a state of depressive mood in mice (Smith et al. 1998), our results suggest that mice suffering from mTBI tend to develop a depressive-like behavior starting from 3 days after the injury.”
BackgroundResultBrain 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
Animal 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
“…the pathologic accumulation of proteins associated with chronic neurodegenerative disease, including amyloid beta and tau (Murai et al., 1998; Smith et al., 1998; Nakagawa et al., 1999, 2000; Hartman et al., 2002; Uryu et al., 2002; Yoshiyama et al., 2005; Abrahamson et al., 2006, 2009;…”
BackgroundSelf-citationOverexpression of Bcl-2 is neuroprotective after experimental brain injury in transgenic mice
Nakamura, M., Raghupathi, R., Merry, D. E., Scherbel, U., Saatman, K. E., & McIntosh, T. K. (1999) · The Journal of Comparative Neurology · doi:10.1002/(sici)1096-9861(19991004)412:4 · Cited by 81 · see citing works
Self-citationGonzalez-Lima, F., Berndt, J. D., Valla, J. E., Games, D., & Reiman, E. M. (2001) · Neuroreport · doi:10.1097/00001756-200108080-00018 · Cited by 62 · see citing works
Wu, Y., Bogale, T. A., Koıstınaho, J., Pizzi, M., Rõlova, T., & Bellucci, A. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02696-z · Cited by 81 · see citing works
“Similar acute A β accumulations accompanied by neuronal death and memory impairment have been reported in APP-transgenic mice subjected to TBI [123].”
BackgroundSuo, Z., Wu, M., Citron, B. A., Wong, G. T., & Festoff, B. W. (2004) · Journal of Neuroscience · doi:10.1523/jneurosci.4856-03.2004 · Cited by 75 · see citing works
Kay, A. D., Petzold, A., Kerr, M., Keir, G., Thompson, E. J., & Nicoll, J. A. R. (2003) · Journal of Neurotrauma · doi:10.1089/089771503770195795 · Cited by 63 · see citing works
“…apoE participates in a coordinated response to brain injury, human in vivo evidence is lacking and the relevance of A b to the process of acute human brain injury is unknown (Horsburgh et al., 1997, 2000a,b; Horsburgh and Nicoll, 1996; Nakagawa et al., 1999; Smith et al., 1998; White et al., 2001).”
Myelin in Alzheimer’s disease: culprit or bystander?
Maitre, M., Jeltsch-David, H., Okechukwu, N. G., Klein, C., Patte-Mensah, C., & Mensah-Nyagan, A.-G. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01554-5 · Cited by 66 · see citing works
Gandy, S., Ikonomović, M. D., Mitsis, E. M., Elder, G. A., Ahlers, S. T., Barth, J. T., Stone, J. R., & DeKosky, S. T. (2014) · Molecular Neurodegeneration · doi:10.1186/1750-1326-9-37 · Cited by 67 · see citing works
Finnie, J. W., & Blumbergs, P. C. (2002) · Veterinary Pathology · doi:10.1354/vp.39-6-679 · Cited by 122 · see citing works
Traumatic brain injury induces biphasic upregulation of ApoE and ApoJ protein in rats
Iwata, A., Browne, K., Chen, X.-H., Yuguchi, T., & Smith, D. H. (2005) · Journal of Neuroscience Research · doi:10.1002/jnr.20607 · Cited by 64 · see citing works
“It has been found previously that TBI in rodent models induces remarkably progressive brain atrophy for at least 1 year postinjury (Smith et al., 1997, 1998; Dixon et al., 1999; Bramlett and Dietrich, 2002).”
BackgroundSelf-citationAtwood, C., Bowen, R. L., Smith, M. A., & Perry, G. L. (2003) · Brain Research Reviews · doi:10.1016/s0165-0173(03)00206-6 · Cited by 64 · see citing works
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Hopkins, R., Tate, D., & Bigler, E. (2005) · Neuropsychology · doi:10.1037/0894-4105.19.2.233 · Cited by 61
Hiltunen, 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
“ciated memory impairment following TBI [101].”
Loane, D. J., Washington, P. M., Vardanian, L., Pocivavsek, A., Hoe, H.-S., Duff, K. E., Cernak, I., Rebeck, G. W., Faden, A. I., & Burns, M. P. (2011) · Journal of Neurotrauma · doi:10.1089/neu.2010.1595 · Cited by 57 · see citing works
“CCI in PDAPP mice causes a brief spike in Ab40 and Ab42, peaking at 2 h post-injury, and returning to baseline by 6 h (Smith et al., 1998).”
Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study
Mielke, M. M., Savica, R., Wiste, H. J., Weigand, S. D., Vemuri, P., Knopman, D. S., Lowe, V. J., Roberts, R. O., Machulda, M. M., Geda, Y. E., et al. (2013) · Neurology · doi:10.1212/01.wnl.0000438229.56094.54 · Cited by 59 · see citing works
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Cheng, W. H., Stukas, S. K., Martens, K. M., Namjoshi, D., Button, E. B., Wilkinson, A., Bashir, A., Robert, J., Cripton, P. A., & Wellington, C. L. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.12.007 · Cited by 46 · see citing works
Ikonomović, M. D., Mi, Z., & Abrahamson, E. E. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.11.003 · Cited by 52 · see citing works
Longhi, 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 49 · see citing works
Self-citationKokiko-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 · see citing works
The role of synaptic activity in the regulation of amyloid beta levels in Alzheimer's disease
Cheng, X., Wu, J., Geng, M., & Xiong, J. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.11.021 · Cited by 48 · see citing works
Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment
Granacher, R. (2003) · doi:10.1201/9780203501740 · Cited by 47
Hånell, A., Clausen, F., Björk, M., Jansson, K., Philipson, O., Nilsson, L. N. G., Hillered, L., Weinreb, P. H., Lee, D. C., McIntosh, T. K., et al. (2010) · Journal of Neurotrauma · doi:10.1089/neu.2009.1255 · Cited by 39 · see citing works
“Following TBI in the mouse, no or only minimal increases of A b have previously been observed (Smith et al., 1998), and our results suggest that accumulation of A b deposition is not a major contributor to this TBI model, nor is A b the likely cause for the impaired cognitive function observed in…”
Self-citationPKC activator therapeutic for mild traumatic brain injury in mice.
Zohar, O., Lavy, R., Zi, X.-M., Nelson, T., Hongpaisan, J., Pick, C. G., & Alkon, D. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.10.001 · Cited by 45 · see citing works
“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.,…”
BackgroundCollins, 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 · see citing works
“PDAPP mice (APPV717F) subjected to CCI prior to the age-related deposition of plaques showed no subsequent change in plaque deposition at two months post-injury (Smith et al., 1998) but a decreased abundance of plaques at eight months post-injury (Nakagawa et al.”
Marchesi, V. T. (2012) · American Journal Of Pathology · doi:10.1016/j.ajpath.2012.03.004 · Cited by 36 · see citing works
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
“…that A (cid:1) deposition may occur more rapidly in predisposed transgenic mice overexpressing APP (Games et al., 1995; Johnson-Wood et al., 1997; Smith et al., 1998) and that overexpression of APP after TBI is a risk factor for the subsequent development of AD (Smith et al., 1998), the…”
Hanzel, D., Trojanowski, J., Johnston, R. F., & Loring, J. (1999) · Nature Biotechnology · doi:10.1038/5225 · Cited by 39 · see citing works
Self-citationFunctional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice
Marklund, N., Morales, D. M., Clausen, F., Hånell, A., Kiwanuka, O., Pitkänen, A., Gimbel, D. A., Philipson, O., Lannfelt, L., Hillered, L., et al. (2009) · Neuroscience · doi:10.1016/j.neuroscience.2009.06.042 · Cited by 38 · see citing works
Self-citationMolecular Pathology of Alzheimer’s Disease and Related Disorders
Ginsberg, S. D., Schmidt, M. L., Crino, P. B., Eberwine, J. H., Lee, V. M. ‐., & Trojanowski, J. Q. (1999) · Cerebral cortex · doi:10.1007/978-1-4615-4885-0_17 · Cited by 38 · see citing works
Self-citationKhodaie, B., Lotfinia, A., Ahmadi, M., Lotfinia, M., Jafarian, M., Karimzadeh, F., Coulon, P.-G. A., & Gorji, A. (2015) · Behavioural Brain Research · doi:10.1016/j.bbr.2014.09.034 · Cited by 37 · see citing works
Animal Models of Traumatically-Induced Dementia
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Gene-Environment Interaction Research and Transgenic Mouse Models of Alzheimer's Disease (Erratum)
Chouliaras, L., Sierksma, A. S. R., Kenis, G., Prickaerts, J., Lemmens, M. A. M., Brasnjevic, I., van Donkelaar, E. L., Martínez‐Martínez, P., Losen, M. H., Baets, M. H. D., et al. (2010) · International Journal of Alzheimer s Disease · doi:10.4061/2010/356862 · Cited by 44 · see citing works
“TBI also resulted in hippocampal neuronal loss one week after injury, which was associated with an increase in hippocampal Aβ40 and Aβ42 [150].”
BackgroundInfluentialWhat Can Rodent Models Tell Us About Cognitive Decline in Alzheimer's Disease?
Davis, S., & Laroche, S. (2003) · Molecular Neurobiology · doi:10.1385/mn:27:3:249 · Cited by 31 · see citing works
Gene-Environment Interaction Research and Transgenic Mouse Models of Alzheimer's Disease
Chouliaras, L., Sierksma, A. S. R., Kenis, G., Prickaerts, J., Lemmens, M. A. M., Brasnjevic, I., van Donkelaar, E. L., Martínez‐Martínez, P., Losen, M. H., Baets, M. H. D., et al. (2010) · International Journal of Alzheimer s Disease · doi:10.4061/2010/859101 · Cited by 30 · see citing works
“TBI also resulted in hippocampal neuronal loss one week after injury, which was associated with an increase in hippocampal Aβ40 and Aβ42 [150].”
BackgroundInfluentialMechanical stress increases brain amyloid β, tau, and α‐synuclein concentrations in wild‐type mice
Levy-Nogueira, M., Hamraz, M., Abolhassani, M., Bigan, E., Lafitte, O., Steyaert, J.-M., Dubois, B., & Schwartz, L. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2017.11.003 · Cited by 26 · see citing works
“Controlled cortical impact injury, in turn, can induce a two to threefold increase in Ab1–42 in APP transgenic mice [29,30] and a 50% increase in Ab1–42 in wild-type mice.”
BackgroundPortbury, S. D., & Adlard, P. A. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-143048 · Cited by 26 · see citing works
“in memory impairment) [67].”
The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma
Elder, G. A., Sosa, M. A. G., Gasperi, R. D., Garcia, G. S. P., Perez, G. M., Abutarboush, R., Kawoos, U., Zhu, C. W., Janssen, W. G. M., Stone, J. R., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25021150 · Cited by 24 · see citing works
- Authors
- Smith, D. H., Nakamura, M., McIntosh, T. K., Wang, J., Rodríguez, A., Chen, X.-H., Raghupathi, R., Saatman, K. E., Clemens, J., Schmidt, M. L., Lee, V. M.-Y., & Trojanowski, J. Q.
- Affiliations
- University of Pennsylvania (US)
- Eli Lilly (United States) (US)
- Corresponding author
- Smith, Douglas H.
- ORCID
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 1998-09
- Volume
- 153
- Issue
- 3
- Pages
- 1005-1010
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1853010
- OpenAlex
- W2028535633
- Cited by
- 143
- References
- 28
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 7 · 2013: 9 · 2012: 3
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health and Human Services (85-23)
- University of Pennsylvania
- National Institute on Aging (AG12527, P01AG011542, AG09215, R01AG012527, P01AG009215, AG 11542)
- National Institute of Neurological Disorders and Stroke (P50NS008803)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- traumatic brain injury, Alzheimer's disease, amyloid precursor protein, amyloid-beta, Aβ40, amyloid-beta 42, memory impairment, cortical impact injury, amyloid plaques
- MeSH terms
- Animals, Brain Injuries, Disease Models, Animal, Female, Hippocampus, Mice, Transgenic, Neurons, Ovariectomy, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Cell Death, Maze Learning, Mice
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