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Journal articles on the topic 'Amyloid precursor protein; traumatic brain injury; sAPPα'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Corrigan, Frances, Robert Vink, Peter C. Blumbergs, Colin L. Masters, Roberto Cappai, and Corinna van den Heuvel. "sAPPα rescues deficits in amyloid precursor protein knockout mice following focal traumatic brain injury." Journal of Neurochemistry 122, no. 1 (May 17, 2012): 208–20. http://dx.doi.org/10.1111/j.1471-4159.2012.07761.x.

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2

Shahim, Pashtun, Yelverton Tegner, Niklas Marklund, Kina Höglund, Erik Portelius, David L. Brody, Kaj Blennow, and Henrik Zetterberg. "Astroglial activation and altered amyloid metabolism in human repetitive concussion." Neurology 88, no. 15 (March 10, 2017): 1400–1407. http://dx.doi.org/10.1212/wnl.0000000000003816.

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Objective:To determine whether postconcussion syndrome (PCS) due to repetitive concussive traumatic brain injury (rcTBI) is associated with CSF biomarker evidence of astroglial activation, amyloid deposition, and blood–brain barrier (BBB) impairment.Methods:A total of 47 participants (28 professional athletes with PCS and 19 controls) were assessed with lumbar puncture (median 1.5 years, range 0.25–12 years after last concussion), standard MRI of the brain, and Rivermead Post-Concussion Symptoms Questionnaire (RPQ). The main outcome measures were CSF concentrations of astroglial activation markers (glial fibrillary acidic protein [GFAP] and YKL-40), markers reflecting amyloid precursor protein metabolism (Aβ38, Aβ40, Aβ42, sAPPα, and sAPPβ), and BBB function (CSF:serum albumin ratio).Results:Nine of the 28 athletes returned to play within a year, while 19 had persistent PCS >1 year. Athletes with PCS >1 year had higher RPQ scores and number of concussions than athletes with PCS <1 year. Median concentrations of GFAP and YKL-40 were higher in athletes with PCS >1 year compared with controls, although with an overlap between the groups. YKL-40 correlated with RPQ score and the lifetime number of concussions. Athletes with rcTBI had lower concentrations of Aβ40 and Aβ42 than controls. The CSF:serum albumin ratio was unaltered.Conclusions:This study suggests that PCS may be associated with biomarker evidence of astroglial activation and β-amyloid (Aβ) dysmetabolism in the brain. There was no clear evidence of Aβ deposition as Aβ40 and Aβ42 were reduced in parallel. The CSF:serum albumin ratio was unaltered, suggesting that the BBB is largely intact in PCS.

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3

Itoh, Tatsuki, Takao Satou, Shozo Nishida, Masahiro Tsubaki, Shigeo Hashimoto, and Hiroyuki Ito. "Expression of amyloid precursor protein after rat traumatic brain injury." Neurological Research 31, no. 1 (February 2009): 103–9. http://dx.doi.org/10.1179/016164108x323771.

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4

Dolinak, David, and Ross Reichard. "An Overview of Inflicted Head Injury in Infants and Young Children, With a Review of β-Amyloid Precursor Protein Immunohistochemistry." Archives of Pathology & Laboratory Medicine 130, no. 5 (May 1, 2006): 712–17. http://dx.doi.org/10.5858/2006-130-712-aooihi.

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Abstract Context.—Inflicted traumatic brain injury of infants and young children results in a complex array of autopsy findings. In many cases, immunostains for β-amyloid precursor protein are used to detect axonal injury. Interpretation of the gross, microscopic, and immunostaining results requires the integration of the many facets of the individual case. Objective.—In this article we review the gross and microscopic findings associated with inflicted traumatic brain injury. The application and interpretation of β-amyloid precursor protein immunostains are discussed and photomicrographs are used to illustrate immunostaining patterns. Data Sources.—The pertinent literature is integrated into a review of the subject. Conclusions.—Inflicted traumatic brain injury often results in subdural, subarachnoid, retinal, and optic nerve sheath hemorrhage. These findings must be interpreted within the entire context of the case. β-Amyloid precursor protein immunostains may be helpful in illustrating the traumatic nature of the injuries in some cases.

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5

Loane, David J., Ana Pocivavsek, Charbel E.-H. Moussa, Rachel Thompson, Yasuji Matsuoka, Alan I. Faden, G. William Rebeck, and Mark P. Burns. "Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury." Nature Medicine 15, no. 4 (March 15, 2009): 377–79. http://dx.doi.org/10.1038/nm.1940.

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6

Leyssen, Maarten, Derya Ayaz, Simon Reeve, Bart De Strooper, and Bassem Hassan. "P1-287 Amyloid precursor protein isessential for survival after traumatic brain injury." Neurobiology of Aging 25 (July 2004): S177. http://dx.doi.org/10.1016/s0197-4580(04)80600-6.

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7

Plummer, Stephanie, Corinna Van den Heuvel, Emma Thornton, Frances Corrigan, and Roberto Cappai. "The Neuroprotective Properties of the Amyloid Precursor Protein Following Traumatic Brain Injury." Aging and Disease 7, no. 2 (2016): 163. http://dx.doi.org/10.14336/ad.2015.0907.

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8

Lewén, Anders, Gui Lin Li, Pelle Nilsson, Yngve Olsson, and Lars Hillered. "Traumatic brain injury in rat produces changes of β-amyloid precursor protein immunoreactivity." NeuroReport 6, no. 2 (January 1995): 357–60. http://dx.doi.org/10.1097/00001756-199501000-00032.

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9

Li, Shan, Guo-Ji Yan, Ya-Xin Tan, Lu-Lu Xue, Ting-Hua Wang, Hao-Ran Zhao, Min-Nan Lu, et al. "Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42." Neural Plasticity 2022 (November 10, 2022): 1–21. http://dx.doi.org/10.1155/2022/3995227.

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Voltage-gated sodium channel beta 2 (Nav2.2 or Navβ2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navβ2 in amyloid-β 1-42- (Aβ1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Navβ2 knockdown restored neuronal viability of Aβ1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including Aβ42, sAPPα, and sAPPβ, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating Aβ degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Navβ2 plays crucial roles in the repair of neuronal injury induced by Aβ1-42 both in vivo and in vitro.

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10

Ma, Junwei, Kai Zhang, Zhimin Wang, and Gang Chen. "Progress of Research on Diffuse Axonal Injury after Traumatic Brain Injury." Neural Plasticity 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/9746313.

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The current work reviews the concept, pathological mechanism, and process of diagnosing of DAI. The pathological mechanism underlying DAI is complicated, including axonal breakage caused by axonal retraction balls, discontinued protein transport along the axonal axis, calcium influx, and calpain-mediated hydrolysis of structural protein, degradation of axonal cytoskeleton network, the changes of transport proteins such as amyloid precursor protein, and changes of glia cells. Based on the above pathological mechanism, the diagnosis of DAI is usually made using methods such as CT, traditional and new MRI, biochemical markers, and neuropsychological assessment. This review provides a basis in literature for further investigation and discusses the pathological mechanism. It may also facilitate improvement of the accuracy of diagnosis for DAI, which may come to play a critical role in breaking through the bottleneck of the clinical treatment of DAI and improving the survival and quality of life of patients through clear understanding of pathological mechanisms and accurate diagnosis.

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11

Smith, Douglas H., Xiao-han Chen, Akira Iwata, and David I. Graham. "Amyloid β accumulation in axons after traumatic brain injury in humans." Journal of Neurosurgery 98, no. 5 (May 2003): 1072–77. http://dx.doi.org/10.3171/jns.2003.98.5.1072.

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Object. Although plaques composed of amyloid β (Aβ) have been found shortly after traumatic brain injury (TBI) in humans, the source for this Aβ has not been identified. In the present study, the authors explored the potential relationship between Aβ accumulation in damaged axons and associated Aβ plaque formation. Methods. The authors performed an immunohistochemical analysis of paraffin-embedded sections of brain from 12 patients who died after TBI and from two control patients by using antibodies selective for Aβ peptides, amyloid precursor protein (APP), and neurofilament (NF) proteins. In nine brain-injured patients, extensive colocalizations of Aβ, APP, and NF protein were found in swollen axons. Many of these immunoreactive axonal profiles were present close to Aβ plaques or were surrounded by Aβ staining, which spread out into the tissue. Immunoreactive profiles were not found in the brains of the control patients. Conclusions. The results of this study indicate that damaged axons can serve as a large reservoir of Aβ, which may contribute to Aβ plaque formation after TBI in humans.

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12

Parikh, Umang, Melissa Williams, Addison Jacobs, Jose A. Pineda, David L. Brody, and Stuart H. Friess. "Delayed Hypoxemia Following Traumatic Brain Injury Exacerbates White Matter Injury." Journal of Neuropathology & Experimental Neurology 75, no. 8 (June 10, 2016): 731–47. http://dx.doi.org/10.1093/jnen/nlw045.

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Abstract Hypoxemia immediately following traumatic brain injury (TBI) has been observed to exacerbate injury. However, it remains unclear whether delayed hypoxemia beyond the immediate postinjury period influences white matter injury. In a retrospective clinical cohort of children aged 4–16 years admitted with severe TBI, 28/74 (35%) patients were found to experience delayed normocarbic hypoxemia within 7 days of admission. Based on these clinical findings, we developed a clinically relevant mouse model of TBI with delayed hypoxemia by exposing 5-week old (adolescent) mice to hypoxic conditions for 30 minutes starting 24 hours after moderate controlled cortical impact (CCI). Injured mice with hypoxemia had increased axonal injury using both β-amyloid precursor protein and NF200 immunostaining in peri-contusional white matter compared with CCI alone. Furthermore, we detected increased peri-contusional white matter tissue hypoxia with pimonidazole and augmented astrogliosis with anti-glial fibrillary acidic protein staining in CCI + delayed hypoxemia compared with CCI alone or sham surgery + delayed hypoxemia. Microglial activation as evidenced by Iba1 staining was not significantly altered by delayed hypoxemia. These clinical and experimental data indicate the prevention or amelioration of delayed hypoxemia effects following TBI may provide a unique opportunity for the development of therapeutic interventions to reduce axonal injury and improve clinical outcomes.

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13

Abrahamson, Eric E., Milos D. Ikonomovic, Caroline Hope, and Steven T. DeKosky. "P1-231 Post-injury increases in NFKB precede changes in amyloid precursor protein and amyloid beta following traumatic brain injury." Neurobiology of Aging 25 (July 2004): S162. http://dx.doi.org/10.1016/s0197-4580(04)80544-x.

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14

Okonkwo, David O., and John T. Povlishock. "An Intrathecal Bolus of Cyclosporin a before Injury Preserves Mitochondrial Integrity and Attenuates Axonal Disruption in Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 19, no. 4 (April 1999): 443–51. http://dx.doi.org/10.1097/00004647-199904000-00010.

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Traumatic brain injury evokes multiple axonal pathologies that contribute to the ultimate disconnection of injured axons. In severe traumatic brain injury, the axolemma is perturbed focally, presumably allowing for the influx of Ca2+ and initiation of Ca2+-sensitive, proaxotomy processes. Mitochondria in foci of axolemmal failure may act as Ca2+ sinks that sequester Ca2+ to preserve low cytoplasmic calcium concentrations. This Ca2+ load within mitochondria, however, may cause colloid osmotic swelling and loss of function by a Ca2+-induced opening of the permeability transition pore. Local failure of mitochondria, in turn, can decrease production of high-energy phosphates necessary to maintain membrane pumps and restore ionic balance in foci of axolemmal permeability change. The authors evaluated the ability of the permeability transition pore inhibitor cyclosporin A (CsA) to prevent mitochondrial swelling in injured axonal segments demonstrating altered axolemmal permeability after impact acceleration injury in rat. At the electron microscopic level, statistically fewer abnormal mitochondria were seen in traumatically injured axons from CsA-pretreated injured animals. Further, this mitochondrial protection translated into axonal protection in a second group of injured rats, whose brains were reacted with antibodies against amyloid precursor protein, a known marker of injured axons. Pretreatment with CsA significantly reduced the number of axons undergoing delayed axotomy, as evidenced by a decrease in the density of amyloid precursor protein-immunoreactive axons. Collectively, these studies demonstrate that CsA protects both mitochondria and the related axonal shaft, suggesting that this agent may be of therapeutic use in traumatic brain injury.

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15

Plummer, Stephanie L., Frances Corrigan, Emma Thornton, Joshua A. Woenig, Robert Vink, Roberto Cappai, and Corinna Van Den Heuvel. "The amyloid precursor protein derivative, APP96-110, is efficacious following intravenous administration after traumatic brain injury." PLOS ONE 13, no. 1 (January 10, 2018): e0190449. http://dx.doi.org/10.1371/journal.pone.0190449.

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16

Ayton, Scott, Moses Zhang, Blaine R. Roberts, Linh Q. Lam, Monica Lind, Catriona McLean, Ashley I. Bush, Tony Frugier, Peter J. Crack, and James A. Duce. "Ceruloplasmin and β-amyloid precursor protein confer neuroprotection in traumatic brain injury and lower neuronal iron." Free Radical Biology and Medicine 69 (April 2014): 331–37. http://dx.doi.org/10.1016/j.freeradbiomed.2014.01.041.

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17

Cartagena, Casandra M., Andrea Mountney, Hye Hwang, Adam Swiercz, Zoe Rammelkamp, Angela M. Boutte, Deborah A. Shear, Frank C. Tortella, and Kara E. Schmid. "Subacute Changes in Cleavage Processing of Amyloid Precursor Protein and Tau following Penetrating Traumatic Brain Injury." PLOS ONE 11, no. 7 (July 18, 2016): e0158576. http://dx.doi.org/10.1371/journal.pone.0158576.

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18

Koob, Andrew O., and Richard B. Borgens. "Polyethylene glycol treatment after traumatic brain injury reduces β-amyloid precursor protein accumulation in degenerating axons." Journal of Neuroscience Research 83, no. 8 (June 2006): 1558–63. http://dx.doi.org/10.1002/jnr.20837.

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19

Thornton, Emma, Robert Vink, Peter C. Blumbergs, and Corinna Van Den Heuvel. "Soluble amyloid precursor protein α reduces neuronal injury and improves functional outcome following diffuse traumatic brain injury in rats." Brain Research 1094, no. 1 (June 2006): 38–46. http://dx.doi.org/10.1016/j.brainres.2006.03.107.

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20

Ciallella, John R., Dorothy G. Flood, Milos D. Ikonomovic, William Paljug, C. Eduard Dixon, Patrick M. Kochanek, Donald W. Marion, and Steven T. DeKosky. "Amyloid precursor protein and amyloid-β-production are altered by caspase inhibition after traumatic brain injury in humanized Aβ mice." Neurobiology of Aging 21 (May 2000): 18. http://dx.doi.org/10.1016/s0197-4580(00)82757-8.

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21

Iino, Morio, Masato Nakatome, Yoshiaki Ogura, Harutoshi Fujimura, Hisanaga Kuroki, Hiromasa Inoue, Yukiko Ino, Tasuku Fujii, Toshiyuki Terao, and Ryoji Matoba. "Real-time PCR quantitation of FE65 a β-amyloid precursor protein-binding protein after traumatic brain injury in rats." International Journal of Legal Medicine 117, no. 3 (April 18, 2003): 153–59. http://dx.doi.org/10.1007/s00414-003-0370-y.

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22

Ciallella, John R., Milos D. Ikonomovic, William R. Paljug, Yetta I. Wilbur, C. Edward Dixon, Patrick M. Kochanek, Donald W. Marion, and Steven T. DeKosky. "Changes in Expression of Amyloid Precursor Protein and Interleukin-1β after Experimental Traumatic Brain Injury in Rats." Journal of Neurotrauma 19, no. 12 (December 2002): 1555–67. http://dx.doi.org/10.1089/089771502762300229.

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23

Graham, D. I., C. Smith, R. Reichard, P. D. Leclercq, and S. M. Gentleman. "Trials and tribulations of using β-amyloid precursor protein immunohistochemistry to evaluate traumatic brain injury in adults." Forensic Science International 146, no. 2-3 (December 2004): 89–96. http://dx.doi.org/10.1016/s0379-0738(03)00274-3.

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24

Itoh, Tatsuki, Takao Satou, Shozo Nishida, Masahiro Tsubaki, Shigeo Hashimoto, and Hiroyuki Ito. "Improvement of cerebral function by anti-amyloid precursor protein antibody infusion after traumatic brain injury in rats." Molecular and Cellular Biochemistry 324, no. 1-2 (January 7, 2009): 191–99. http://dx.doi.org/10.1007/s11010-008-0013-1.

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25

Fidan, Emin, Lesley M. Foley, Lee Ann New, Henry Alexander, Patrick M. Kochanek, T. Kevin Hitchens, and Hülya Bayır. "Metabolic and Structural Imaging at 7 Tesla After Repetitive Mild Traumatic Brain Injury in Immature Rats." ASN Neuro 10 (January 2018): 175909141877054. http://dx.doi.org/10.1177/1759091418770543.

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Mild traumatic brain injury (mTBI) in children is a common and serious public health problem. Traditional neuroimaging findings in children who sustain mTBI are often normal, putting them at risk for repeated mTBI (rmTBI). There is a need for more sensitive imaging techniques capable of detecting subtle neurophysiological alterations after injury. We examined neurochemical and white matter changes using diffusion tensor imaging of the whole brain and proton magnetic resonance spectroscopy of the hippocampi at 7 Tesla in 18-day-old male rats at 7 days after mTBI and rmTBI. Traumatic axonal injury was assessed by beta-amyloid precursor protein accumulation using immunohistochemistry. A significant decrease in fractional anisotropy and increase in axial and radial diffusivity were observed in several brain regions, especially in white matter regions, after a single mTBI versus sham and more prominently after rmTBI. In addition, we observed accumulation of beta-amyloid precursor protein in the external capsule after mTBI and rmTBI. mTBI and rmTBI reduced the N-acetylaspartate/creatine ratio (NAA/Cr) and increased the myoinositol/creatine ratio (Ins/Cr) versus sham. rmTBI exacerbated the reduction in NAA/Cr versus mTBI. The choline/creatine (Cho/Cr) and (lipid/Macro Molecule 1)/creatine (Lip/Cr) ratios were also decreased after rmTBI versus sham. Diffusion tensor imaging findings along with the decrease in Cho and Lip after rmTBI may reflect damage to axonal membrane. NAA and Ins are altered at 7 days after mTBI and rmTBI likely reflecting neuro-axonal damage and glial response, respectively. These findings may be relevant to understanding the extent of disability following mTBI and rmTBI in the immature brain and may identify possible therapeutic targets.

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26

Li, Shihong, Toshihiko Kuroiwa, Satoru Ishibashi, Liyuan Sun, Shu Endo, and Kikuo Ohno. "Transient cognitive deficits are associated with the reversible accumulation of amyloid precursor protein after mild traumatic brain injury." Neuroscience Letters 409, no. 3 (December 2006): 182–86. http://dx.doi.org/10.1016/j.neulet.2006.09.054.

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27

Acosta, Sandra A., Naoki Tajiri, Paul R. Sanberg, Yuji Kaneko, and Cesar V. Borlongan. "Increased Amyloid Precursor Protein and Tau Expression Manifests as Key Secondary Cell Death in Chronic Traumatic Brain Injury." Journal of Cellular Physiology 232, no. 3 (October 19, 2016): 665–77. http://dx.doi.org/10.1002/jcp.25629.

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28

Corrigan, Frances, Robert Vink, Peter C. Blumbergs, Colin L. Masters, Roberto Cappai, and Corinna van den Heuvel. "Characterisation of the effect of knockout of the amyloid precursor protein on outcome following mild traumatic brain injury." Brain Research 1451 (April 2012): 87–99. http://dx.doi.org/10.1016/j.brainres.2012.02.045.

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29

Van den Heuvel, Corinna, Peter C. Blumbergs, John W. Finnie, Jim Manavis, Nigel R. Jones, Peter L. Reilly, and Rosemarie A. Pereira. "Upregulation of Amyloid Precursor Protein Messenger RNA in Response to Traumatic Brain Injury: An Ovine Head Impact Model." Experimental Neurology 159, no. 2 (October 1999): 441–50. http://dx.doi.org/10.1006/exnr.1999.7150.

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30

Almenar-Queralt, Angels, Rodrigo dos Santos Chaves, Ester J. Kwon, and Sameer B. Shah. "Heads Up! Interlinked Amyloidogenic and Axonal Transport Pathways in Concussion-Induced Neurodegeneration." Neuroscience Insights 17 (January 2022): 263310552211296. http://dx.doi.org/10.1177/26331055221129641.

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Mild traumatic brain injury (mTBI), a condition in which brain function is transiently disrupted by a mechanical force, is a major risk factor for developing Alzheimer’s disease (AD) and other neurodegenerative conditions. In this commentary, we summarize recent findings in human neurons derived from induced pluripotent stem cells, detailing early neuronal events following mild injury that may seed future neurodegeneration. In particular, we discuss interlinked relationships between mTBI and several biological pathways hypothesized to underlie AD progression, including amyloidogenic cleavage of amyloid precursor protein (APP), impairment of axonal transport, and the development of APP-associated axonal swellings. We also describe the implications of these findings for future mechanistic and translational studies.

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31

Chen, Szu-Fu, Hugh K. Richards, Piotr Smielewski, Peter Johnström, Raymond Salvador, John D. Pickard, and Neil G. Harris. "Relationship between Flow-Metabolism Uncoupling and Evolving Axonal Injury after Experimental Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 24, no. 9 (September 2004): 1025–36. http://dx.doi.org/10.1097/01.wcb.0000129415.34520.47.

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Blood flow-metabolism uncoupling is a well-documented phenomenon after traumatic brain injury, but little is known about the direct consequences for white matter. The aim of this study was to quantitatively assess the topographic interrelationship between local cerebral blood flow (LCBF) and glucose metabolism (LCMRglc) after controlled cortical impact injury and to determine the degree of correspondence with the evolving axonal injury. LCMRglc and LCBF measurements were obtained at 3 hours in the same rat from 18F-fluorodeoxyglucose and 14C-iodoantipyrine coregistered autoradiographic images, and compared to the density of damaged axonal profiles in adjacent sections and in an additional group at 24 hours using beta-amyloid precursor protein (ß-APP) immunohistochemistry. LCBF was significantly reduced over the ipsilateral hemisphere by 48 ± 15% compared with sham-controls, whereas LCMRglc was unaffected, apart from foci of elevated LCMRglc in the contusion margin. Flow-metabolism was uncoupled, indicated by a significant 2-fold elevation in the LCMRglc/LCBF ratio within most ipsilateral structures. There was a significant increase in ß-APP-stained axons from 3 to 24 hours, which was negatively correlated with LCBF and positively correlated with the LCMRglc/LCBF ratio at 3 hours in the cingulum and corpus callosum. Our study indicates a possible dependence of axonal outcome on flow-metabolism in the acute injury stage.

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32

Shishido, Hajime, Masaki Ueno, Kana Sato, Masahisa Matsumura, Yasunori Toyota, Yutaka Kirino, Takashi Tamiya, Nobuyuki Kawai, and Yasushi Kishimoto. "Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-β Deposition and Acute Cognitive Deficits in Mice." Behavioural Neurology 2019 (March 3, 2019): 1–8. http://dx.doi.org/10.1155/2019/3248519.

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There has been growing awareness of the correlation between an episode of traumatic brain injury (TBI) and the development of Alzheimer’s disease (AD) later in life. It has been reported that TBI accelerated amyloid-β (Aβ) pathology and cognitive decline in the several lines of AD model mice. However, the short-term and long-term effects of TBI by the weight-drop method on amyloid-β pathology and cognitive performance are unclear in wild-type (WT) mice. Hence, we examined AD-related histopathological changes and cognitive impairment after TBI in wild-type C57BL6J mice. Five- to seven-month-old WT mice were subjected to either TBI by the weight-drop method or a sham treatment. Seven days after TBI, the WT mice exhibited significantly lower spatial learning than the sham-treated WT mice. However, 28 days after TBI, the cognitive impairment in the TBI-treated WT mice recovered. Correspondingly, while significant amyloid-β (Aβ) plaques and amyloid precursor protein (APP) accumulation were observed in the TBI-treated mouse hippocampus 7 days after TBI, the Aβ deposition was no longer apparent 28 days after TBI. Thus, TBI induced transient amyloid-β deposition and acute cognitive impairments in the WT mice. The present study suggests that the TBI could be a risk factor for acute cognitive impairment even when genetic and hereditary predispositions are not involved. The system might be useful for evaluating and developing a pharmacological treatment for the acute cognitive deficits.

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33

VAN DEN HEUVEL, CORINNA, JOHN W. FINNIE, PETER C. BLUMBERGS, JIM MANAVIS, NIGEL R. JONES, PETER L. REILLY, and ROSEMARIE A. PEREIRA. "Upregulation of Neuronal Amyloid Precursor Protein (APP) and APP mRNA Following Magnesium Sulphate (MgSO4) Therapy in Traumatic Brain Injury." Journal of Neurotrauma 17, no. 11 (November 2000): 1041–53. http://dx.doi.org/10.1089/neu.2000.17.1041.

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34

Losurdo, Michela, Johan Davidsson, and Mattias K. Sköld. "Diffuse Axonal Injury in the Rat Brain: Axonal Injury and Oligodendrocyte Activity Following Rotational Injury." Brain Sciences 10, no. 4 (April 10, 2020): 229. http://dx.doi.org/10.3390/brainsci10040229.

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Traumatic brain injury (TBI) commonly results in primary diffuse axonal injury (DAI) and associated secondary injuries that evolve through a cascade of pathological mechanisms. We aim at assessing how myelin and oligodendrocytes react to head angular-acceleration-induced TBI in a previously described model. This model induces axonal injuries visible by amyloid precursor protein (APP) expression, predominantly in the corpus callosum and its borders. Brain tissue from a total of 27 adult rats was collected at 24 h, 72 h and 7 d post-injury. Coronal sections were prepared for immunohistochemistry and RNAscope® to investigate DAI and myelin changes (APP, MBP, Rip), oligodendrocyte lineage cell loss (Olig2), oligodendrocyte progenitor cells (OPCs) (NG2, PDGFRa) and neuronal stress (HSP70, ATF3). Oligodendrocytes and OPCs numbers (expressed as percentage of positive cells out of total number of cells) were measured in areas with high APP expression. Results showed non-statistically significant trends with a decrease in oligodendrocyte lineage cells and an increase in OPCs. Levels of myelination were mostly unaltered, although Rip expression differed significantly between sham and injured animals in the frontal brain. Neuronal stress markers were induced at the dorsal cortex and habenular nuclei. We conclude that rotational injury induces DAI and neuronal stress in specific areas. We noticed indications of oligodendrocyte death and regeneration without statistically significant changes at the timepoints measured, despite indications of axonal injuries and neuronal stress. This might suggest that oligodendrocytes are robust enough to withstand this kind of trauma, knowledge important for the understanding of thresholds for cell injury and post-traumatic recovery potential.

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35

Oda, Yasutaka, Guoyi Gao, Enoch P. Wei, and John T. Povlishock. "Combinational Therapy Using Hypothermia and the Immunophilin Ligand FK506 to Target Altered Pial Arteriolar Reactivity, Axonal Damage, and Blood–Brain Barrier Dysfunction after Traumatic Brain Injury in Rat." Journal of Cerebral Blood Flow & Metabolism 31, no. 4 (December 15, 2010): 1143–54. http://dx.doi.org/10.1038/jcbfm.2010.208.

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This study evaluated the utility of combinational therapy, coupling delayed posttraumatic hypothermia with delayed FK506 administration, on altered cerebral vascular reactivity, axonal injury, and blood–brain barrier (BBB) disruption seen following traumatic brain injury (TBI). Animals were injured, subjected to various combinations of hypothermic/FK506 intervention, and equipped with cranial windows to assess pial vascular reactivity to acetylcholine. Animals were then processed with antibodies to the amyloid precursor protein and immunoglobulin G to assess axonal injury and BBB disruption, respectively. Animals were assigned to five groups: (1) sham injury plus delayed FK506, (2) TBI, (3) TBI plus delayed hypothermia, (4) TBI plus delayed FK506, and (5) TBI plus delayed hypothermia with FK506. Sham injury plus FK506 had no impact on vascular reactivity, axonal injury, or BBB disruption. Traumatic brain injury induced dramatic axonal injury and altered pial vascular reactivity, while triggering local BBB disruption. Delayed hypothermia or FK506 after TBI provided limited protection. However, TBI with combinational therapy achieved significantly enhanced vascular and axonal protection, with no BBB protection. This study shows the benefits of combinational therapy, using posttraumatic hypothermia with FK506 to attenuate important features of TBI. This suggests that hypothermia not only protects but also extends the therapeutic window for improved FK506 efficacy.

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Lewén, Anders, Gui Lin Li, Yngve Olsson, and Lars Hillered. "Changes in microtubule-associated protein 2 and amyloid precursor protein immunoreactivity following traumatic brain injury in rat: influence of MK-801 treatment." Brain Research 719, no. 1-2 (May 1996): 161–71. http://dx.doi.org/10.1016/0006-8993(96)00081-9.

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Corrigan, Frances, Chi L. L. Pham, Robert Vink, Peter C. Blumbergs, Colin L. Masters, Corinna van den Heuvel, and Roberto Cappai. "The neuroprotective domains of the amyloid precursor protein, in traumatic brain injury, are located in the two growth factor domains." Brain Research 1378 (March 2011): 137–43. http://dx.doi.org/10.1016/j.brainres.2010.12.077.

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Washington, Patricia M., and Mark P. Burns. "The Effect of the APOE4 Gene on Accumulation of Aβ 40 After Brain Injury Cannot Be Reversed by Increasing apoE4 Protein." Journal of Neuropathology & Experimental Neurology 75, no. 8 (June 11, 2016): 770–78. http://dx.doi.org/10.1093/jnen/nlw049.

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Abstract The apolipoprotein E (apoE) protein is involved in clearance of β-amyloid (Aβ) from the brain; and the APOE4 gene is associated with Aβ plaque formation in humans following traumatic brain injury (TBI). Here, we examined the association between apoE and Aβ 40 after experimental TBI and the effects of APOE alleles on this relationship. We report a biphasic response of soluble apoE protein after TBI with an acute reduction at 1 day postinjury followed by an increase at 7 days postinjury. TBI-induced Aβ 40 levels decreased as soluble apoE levels increased. In APOE4 mice there was a diminished apoE response to TBI that corresponded to prolonged accumulation of TBI-induced Aβ 40 versus that in APOE3 mice. Amyloid precursor protein processing was similar in APOE3 and APOE4 mice suggesting that impaired clearance was responsible for the abnormal accumulation of Aβ 40 in the latter. Treatment of APOE4 mice with bexarotene for 7 days increased apoE4 protein levels but was not sufficient to reduce TBI-induced Aβ 40 . Thus, rapid clearance of TBI-induced Aβ 40 occurs in mice but these pathways are impaired in APOE4 carriers. These data may help explain the deposition of Aβ in APOE4 carriers and the increased incidence of brain Aβ plaques following TBI.

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Zhang, Yanlu, Michael Chopp, Yuling Meng, Zheng Gang Zhang, Edith Doppler, Stefan Winter, Timothy Schallert, Asim Mahmood, and Ye Xiong. "Cerebrolysin improves cognitive performance in rats after mild traumatic brain injury." Journal of Neurosurgery 122, no. 4 (April 2015): 843–55. http://dx.doi.org/10.3171/2014.11.jns14271.

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OBJECT Long-term memory deficits occur after mild traumatic brain injuries (mTBIs), and effective treatment modalities are currently unavailable. Cerebrolysin, a peptide preparation mimicking the action of neurotrophic factors, has beneficial effects on neurodegenerative diseases and brain injuries. The present study investigated the long-term effects of Cerebrolysin treatment on cognitive function in rats after mTBI. METHODS Rats subjected to closed-head mTBI were treated with saline (n = 11) or Cerebrolysin (2.5 ml/kg, n = 11) starting 24 hours after injury and then daily for 28 days. Sham animals underwent surgery without injury (n = 8). To evaluate cognitive function, the modified Morris water maze (MWM) test and a social odor–based novelty recognition task were performed after mTBI. All rats were killed on Day 90 after mTBI, and brain sections were immunostained for histological analyses of amyloid precursor protein (APP), astrogliosis, neuroblasts, and neurogenesis. RESULTS Mild TBI caused long-lasting cognitive memory deficits in the MWM and social odor recognition tests up to 90 days after injury. Compared with saline treatment, Cerebrolysin treatment significantly improved both long-term spatial learning and memory in the MWM test and nonspatial recognition memory in the social odor recognition task up to 90 days after mTBI (p < 0.05). Cerebrolysin significantly increased the number of neuroblasts and promoted neurogenesis in the dentate gyrus, and it reduced APP levels and astrogliosis in the corpus callosum, cortex, dentate gyrus, CA1, and CA3 regions (p < 0.05). CONCLUSIONS These results indicate that Cerebrolysin treatment of mTBI improves long-term cognitive function, and this improvement may be partially related to decreased brain APP accumulation and astrogliosis as well as increased neuroblasts and neurogenesis.

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Kim, Jung H., James A. Goodrich, Robert Situ, Amedeo Rapuano, Hoby Hetherington, Fu Du, Steve Parks, et al. "Periventricular White Matter Alterations From Explosive Blast in a Large Animal Model: Mild Traumatic Brain Injury or “Subconcussive” Injury?" Journal of Neuropathology & Experimental Neurology 79, no. 6 (April 7, 2020): 605–17. http://dx.doi.org/10.1093/jnen/nlaa026.

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Abstract The neuropathology of mild traumatic brain injury in humans resulting from exposure to explosive blast is poorly understood as this condition is rarely fatal. A large animal model may better reflect the injury patterns in humans. We investigated the effect of explosive blasts on the constrained head minimizing the effects of whole head motion. Anesthetized Yucatan minipigs, with body and head restrained, were placed in a 3-walled test structure and exposed to 1, 2, or 3 explosive blast shock waves of the same intensity. Axonal injury was studied 3 weeks to 8 months postblast using β-amyloid precursor protein immunohistochemistry. Injury was confined to the periventricular white matter as early as 3–5 weeks after exposure to a single blast. The pattern was also present at 8 months postblast. Animals exposed to 2 and 3 blasts had more axonal injury than those exposed to a single blast. Although such increases in axonal injury may relate to the longer postblast survival time, it may also be due to the increased number of blast exposures. It is possible that the injury observed is due to a condition akin to mild traumatic brain injury or subconcussive injury in humans, and that periventricular injury may have neuropsychiatric implications.

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Melton, L. M., E. W. Hillhouse, A. J. Gunn, J. M. Candy, and P. M. Sharples. "Changes in interleukin-1 beta (IL-1 beta) and amyloid precursor protein (APP) expression following traumatic brain injury in the rat." Journal of Neuroimmunology 54, no. 1-2 (October 1994): 182. http://dx.doi.org/10.1016/0165-5728(94)90441-3.

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Jackson, Travis C., Lina Du, Keri Janesko-Feldman, Vincent A. Vagni, Cameron Dezfulian, Samuel M. Poloyac, Edwin K. Jackson, Robert SB Clark, and Patrick M. Kochanek. "The Nuclear Splicing Factor RNA Binding Motif 5 Promotes Caspase Activation in Human Neuronal Cells, and Increases after Traumatic Brain Injury in Mice." Journal of Cerebral Blood Flow & Metabolism 35, no. 4 (January 14, 2015): 655–66. http://dx.doi.org/10.1038/jcbfm.2014.242.

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Splicing factors (SFs) coordinate nuclear intron/exon splicing of RNA. Splicing factor disturbances can cause cell death. RNA binding motif 5 (RBM5) and 10 (RBM10) promote apoptosis in cancer cells by activating detrimental alternative splicing of key death/survival genes. The role(s) of RBM5/10 in neurons has not been established. Here, we report that RBM5 knockdown in human neuronal cells decreases caspase activation by staurosporine. In contrast, RBM10 knockdown augments caspase activation. To determine whether brain injury alters RBM signaling, we measured RBM5/10 protein in mouse cortical/hippocampus homogenates after controlled cortical impact (CCI) traumatic brain injury (TBI) plus hemorrhagic shock (CCI+HS). The RBM5/10 staining was higher 48 to 72 hours after injury and appeared to be increased in neuronal nuclei of the hippocampus. We also measured levels of other nuclear SFs known to be essential for cellular viability and report that splicing factor 1 (SF1) but not splicing factor 3A (SF3A) decreased 4 to 72 hours after injury. Finally, we confirm that RBM5/10 regulate protein expression of several target genes including caspase-2, cellular FLICE-like inhibitory protein (c-FLIP), LETM1 Domain-Containing Protein 1 (LETMD1), and amyloid precursor-like protein 2 (APLP2) in neuronal cells. Knockdown of RBM5 appeared to increase expression of c-FLIP(s), LETMD1, and APLP2 but decrease caspase-2.

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Rahaman, Petra, and Marc R. Del Bigio. "Histology of Brain Trauma and Hypoxia-Ischemia." Academic Forensic Pathology 8, no. 3 (August 31, 2018): 539–54. http://dx.doi.org/10.1177/1925362118797728.

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Forensic pathologists encounter hypoxic-ischemic (HI) brain damage or traumatic brain injuries (TBI) on an almost daily basis. Evaluation of the findings guides decisions regarding cause and manner of death. When there are gross findings of brain trauma, the cause of death is often obvious. However, microscopic evaluation should be used to augment the macroscopic diagnoses. Histology can be used to seek evidence for TBI in the absence of gross findings, e.g., in the context of reported or suspected TBI. Estimating the survival interval after an insult is often of medicolegal interest; this requires targeted tissue sampling and careful histologic evaluation. Retained tissue blocks serve as forensic evidence and also provide invaluable teaching and research material. In certain contexts, histology can be used to demonstrate nontraumatic causes of seemingly traumatic lesions. Macroscopic and histologic findings of brain trauma can be confounded by concomitant HI brain injury when an individual survives temporarily after TBI. Here we review the histologic approaches for evaluating TBI, hemorrhage, and HI brain injury. Amyloid precursor protein (APP) immunohistochemistry is helpful for identifying damaged axons, but patterns of damage cannot unambiguously distinguish TBI from HI. The evolution of hemorrhagic lesions will be discussed in detail; however, timing of any lesion is at best approximate. It is important to recognize artifactual changes (e.g., dark neurons) that can resemble HI damage. Despite the shortcomings, histology is a critical adjunct to the gross examination of brains.

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Zhang, Jian, Zhaoqian Teng, Yunping Song, Mei Hu, and Chu Chen. "Inhibition of Monoacylglycerol Lipase Prevents Chronic Traumatic Encephalopathy-like Neuropathology in a Mouse Model of Repetitive Mild Closed Head Injury." Journal of Cerebral Blood Flow & Metabolism 35, no. 3 (March 2015): 443–53. http://dx.doi.org/10.1038/jcbfm.2014.216.

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Emerging evidence suggests that the risk of developing chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease, is significantly increased in military personnel and contact sports players who have been exposed to repetitive trauma brain injury (TBI). Unfortunately there are no effective medications currently available for prevention and treatment of CTE. Here we demonstrate that inhibition of monoacylglycerol lipase (MAGL), the key enzyme that metabolizes the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, significantly reduced CTE-like neuropathologic changes in a mouse model of repetitive mild closed head injury (rmCHI). Inhibition of 2-AG metabolism promoted neurologic recovery following rmCHI and reduced proinflammatory cytokines, astroglial reactivity, expression of amyloid precursor protein and the enzymes that make Aβ, as well as formation of Aβ. Importantly, neurodegeneration, TDP-43 protein aggregation, and tau phosphorylation, which are the neuropathologic hallmarks of CTE, were significantly suppressed by MAGL inactivation. Furthermore, alterations in expression of glutamate receptor subunits and impairments in basal synaptic transmission, long-term synaptic plasticity, and spatial learning and memory were recovered by inhibition of 2-AG metabolism in animals exposed to rmCHI. Our results suggest that MAGL inhibition, which boosts 2-AG and reduces 2-AG metabolites prostaglandins in the brain, may lead to a new therapy for CTE.

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Corrigan, Frances, Emma Thornton, Laila C. Roisman, Anna V. Leonard, Robert Vink, Peter C. Blumbergs, Corinna van den Heuvel, and Roberto Cappai. "The neuroprotective activity of the amyloid precursor protein against traumatic brain injury is mediated via the heparin binding site in residues 96-110." Journal of Neurochemistry 128, no. 1 (August 28, 2013): 196–204. http://dx.doi.org/10.1111/jnc.12391.

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Koizumi, Hiroyasu, and John T. Povlishock. "Posttraumatic hypothermia in the treatment of axonal damage in an animal model of traumatic axonal injury." Journal of Neurosurgery 89, no. 2 (August 1998): 303–9. http://dx.doi.org/10.3171/jns.1998.89.2.0303.

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Object. Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically, this protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBI in rats. Methods. Male Sprague—Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32°C for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the amyloid precursor protein (APP), a marker of axonal injury. The density of APP-marked damaged axons within the corticospinal tract at the pontomedullary junction was calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05). Conclusions. The authors infer from these findings that early as well as delayed posttraumatic hypothermia results in substantial protection in TBI, at least in terms of the injured axons.

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Zhang, Yanlu, Michael Chopp, Zheng Gang Zhang, Yi Zhang, Li Zhang, Mei Lu, Talan Zhang, et al. "Cerebrolysin Reduces Astrogliosis and Axonal Injury and Enhances Neurogenesis in Rats After Closed Head Injury." Neurorehabilitation and Neural Repair 33, no. 1 (November 30, 2018): 15–26. http://dx.doi.org/10.1177/1545968318809916.

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Background. Cerebrolysin is a neuropeptide preparation with neuroprotective and neurotrophic properties. Our previous study demonstrates that cerebrolysin significantly improves functional recovery in rats after mild traumatic brain injury (mTBI). Objective. To determine histological outcomes associated with therapeutic effects of cerebrolysin on functional recovery after TBI. Methods. In this prospective, randomized, blinded, and placebo-controlled study, adult Wistar rats with mild TBI induced by a closed head impact were randomly assigned to one of the cerebrolysin dose groups (0.8, 2.5, 7.5 mL/kg) or placebo, which were administered 4 hours after TBI and then daily for 10 consecutive days. Functional tests assessed cognitive, behavioral, motor, and neurological performance. Study end point was day 90 after TBI. Brains were processed for histological tissue analyses of astrogliosis, axonal injury, and neurogenesis. Results. Compared with placebo, cerebrolysin significantly reduced amyloid precursor protein accumulation, astrogliosis, and axonal damage in various brain regions and increased the number of neuroblasts and neurogenesis in the dentate gyrus. There was a significant dose effect of cerebrolysin on functional outcomes at 3 months after injury compared with saline treatment. Cerebrolysin at a dose of ⩾0.8 mL/kg significantly improved cognitive function, whereas at a dose of ⩾2.5 mL/kg, cerebrolysin also significantly improved sensorimotor function at various time points. There were significant correlations between multiple histological and functional outcomes 90 days after mTBI. Conclusions. Our findings demonstrate that cerebrolysin reduces astrogliosis and axonal injury and promotes neurogenesis, which may contribute to improved functional recovery in rats with mTBI.

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Kishimoto, Yasushi, Hajime Shishido, Mayumi Sawanishi, Yasunori Toyota, Masaki Ueno, Takashi Kubota, Yutaka Kirino, Takashi Tamiya, and Nobuyuki Kawai. "Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer׳s disease." Data in Brief 9 (December 2016): 62–67. http://dx.doi.org/10.1016/j.dib.2016.08.041.

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Gao, Guoyi, Yasutaka Oda, Enoch P. Wei, and John T. Povlishock. "The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat." Journal of Cerebral Blood Flow & Metabolism 30, no. 3 (November 11, 2009): 628–37. http://dx.doi.org/10.1038/jcbfm.2009.235.

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This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.

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Gleckman, Aaron M., Michael D. Bell, Richard J. Evans, and Thomas W. Smith. "Diffuse Axonal Injury in Infants With Nonaccidental Craniocerebral Trauma." Archives of Pathology & Laboratory Medicine 123, no. 2 (February 1, 1999): 146–51. http://dx.doi.org/10.5858/1999-123-0146-daiiiw.

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Abstract Objective.—Accurate identification of diffuse axonal injury is important in the forensic investigation of infants who have died from traumatic brain injury. β-Amyloid precursor protein (β-APP) immunohistochemical staining is highly sensitive in identifying diffuse axonal injury. However, the effectiveness of this method in brain-injured infants has not been well established. The present study was undertaken to assess the utility of β-APP immunohistochemistry in detecting diffuse axonal injury in infants with either shaken baby syndrome or blunt head trauma. Materials and Methods.—Archival formalin-fixed, paraffin-embedded blocks from infants (<1 year old) with shaken baby syndrome (7 cases) and blunt head trauma (3) and blocks from 7 control cases that included nontraumatic cerebral edema (1), acute hypoxic-ischemic encephalopathy (1), and normal brain (5) were immunostained for β-APP. A semiquantitative assessment of the severity of axonal staining was made. Corresponding hematoxylin-eosin–stained sections were examined for the presence of axonal swellings. Results.—Immunostaining for β-APP identified diffuse axonal injury in 5 of 7 infants with shaken baby syndrome and 2 of 3 infants with blunt head trauma. Immunoreactive axons were easily identified and were present in the majority of the sections examined. By contrast, hematoxylin-eosin staining revealed axonal swellings in only 3 of 7 infants with shaken baby syndrome and 1 of 3 infants with blunt head trauma. Most of these sections had few if any visible axonal swellings, which were often overlooked on initial review of the slides. No β-APP immunoreactivity was observed in any of the 7 control cases. Conclusions.—Immunostaining for β-APP can easily and reliably identify diffuse axonal injury in infants younger than 1 year and is considerably more sensitive than routine hematoxylin-eosin staining. We recommend its use in the forensic evaluation of infants with fatal craniocerebral trauma.

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