The DOI matches its Crossref record; 32 of the 75 references it cites were found in a registry or an index.
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
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516 · cited 1×
“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
Gennarelli, T. A., Thibault, L. E., Adams, J. H., Graham, D. I., Thompson, C. J., & Marcincin, R. P. (1982) · Annals of Neurology · doi:10.1002/ana.410120611 · Cited by 1,528
Self-citationDiffuse axonal injury in head injury: definition, diagnosis and grading
Adams, J. H., Doyle, D., Ford, I., Gennarelli, T. A., Graham, D. I., & Mclellan, D. R. (1989) · Histopathology · doi:10.1111/j.1365-2559.1989.tb03040.x · Cited by 1,176 · cited 1×
“The extent of DA1 increases in parallel with the severity of TBI and correlates with measures of postinjury morbidity and mortality (Gennarelli et al., 1982a; Pilz, 1983; Adams et al., 1989; Povlishock, 1992; Povlishock et al., 1992; Blumbergs et al., 1994).”
BackgroundSelf-citationTraumatic brain injury in the rat: characterization of a lateral fluid-percussion model.
McIntosh, T., Vink, R., Noble, L., Yamakami, I., Fernyak, S., Soares, H., & Faden, A. (1989) · Neuroscience · doi:10.1016/0306-4522(89)90247-9 · Cited by 1,147 · cited 2×
“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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Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport.
Koo, E. H., Sisodia, S. S., Archer, D. R., Martin, L. J., Weidemann, A., Beyreuther, K., Fischer, P., Masters, C. L., & Price, D. L. (1990) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.87.4.1561 · Cited by 733 · cited 2×
“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.”
BackgroundMortimer, J. A., Van Duijn, C. M., Chandra, V, Fratiglioni, L., Graves, A. B., Heyman, A., Jorm, A. F., Kokmen, E., Kondo, K., Rocca, W. A., et al. (1991) · International Journal of Epidemiology · doi:10.1093/ije/20.supplement_2.s28 · Cited by 594
Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations.
Cortez, S., McIntosh, T., & Noble, L. (1989) · Brain Research · doi:10.1016/0006-8993(89)91190-6 · Cited by 481 · cited 3×
“…sections were stained with toluidine blue for verification of and comparison with previously established patterns of post-traumatic neuronal loss (Cortez et al., 1989; Smith et al., 1991; Hicks et al. In the medial thalamus at 1 hr after injury, accumulations of APP/APLP were detected…”
BackgroundMethodInfluentialSelf-citationTraumatically Induced Axonal Injury: Pathogenesis and Pathobiological Implications
Povlishock, J. T. (1991) · Brain Pathology · doi:10.1111/j.1750-3639.1991.tb00050.x · Cited by 453
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Cited by
Sorted by citations
Items 201–215 of 215
Genetic influences and neuropathological sequelae of repetitive brain injury
Laskowitz, D. T., & Dawson, H. (2014) · Annals of Neurology · doi:10.1002/ana.24057 · Cited by 3
“Another limitation in the clinical translation of these findings is that murine TBI models utilizing wild-type mice do not demonstrate amyloid deposition as a function of age or injury.(3) This is particularly important given seminal observations that amyloid–tau interactions may mediate neurotoxicity and subsequent n…”
BackgroundExpression and Cerebral Function of Amyloid Precursor Protein After Rat Traumatic Brain Injury
Itoh, T., Imano, M., Nishida, S., Tsubaki, M., Hashimoto, S., Ito, A., & Satou, T. (2011) · InTech eBooks · doi:10.5772/18814 · Cited by 2
Disease, transplantation and regeneration
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Lovett, S. J. (2017) · doi:10.4225/23/5953466046528
“APP is significantly upregulated in neurons and reactive astrocytes following TBI and SCI (Otsuka et al., 1991; Blumbergs et al., 1994; Li et al., 1995; Pierce et al., 1996; Introduction 31 Bramlett et al., 1997; Van den Heuvel et al., 1999; Kobayashi et al., 2010).”
BackgroundNamjoshi, D. (2015) · doi:10.14288/1.0167688
“The proposed molecular mechanism of DAI and subsequent Aβ 32 accumulation are depicted in Figure 1.5.”
BackgroundInfluentialSchultz, V. (2015) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-4890
Nakagawa (1999) · doi:10.1002/(sici)1096-9861(19990830)411:3
Self-citationA unifying hypothesis of alzheimer’s disease: III—Risk factors
Heininger, K. (2000) · Human Psychopharmacology: Clinical and Experimental · doi:10.1002/(sici)1099-1077(200001)15:1
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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