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Article ; Online: The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.

Elder, Gregory A / Gama Sosa, Miguel A / De Gasperi, Rita / Perez Garcia, Georgina / Perez, Gissel M / Abutarboush, Rania / Kawoos, Usmah / Zhu, Carolyn W / Janssen, William G M / Stone, James R / Hof, Patrick R / Cook, David G / Ahlers, Stephen T

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: Blast-induced neurotrauma has received much attention over the past decade. Vascular injury occurs early following blast exposure. Indeed, in animal models that approximate human mild traumatic brain injury or subclinical blast exposure, vascular ... ...

Abstract	Blast-induced neurotrauma has received much attention over the past decade. Vascular injury occurs early following blast exposure. Indeed, in animal models that approximate human mild traumatic brain injury or subclinical blast exposure, vascular pathology can occur in the presence of a normal neuropil, suggesting that the vasculature is particularly vulnerable. Brain endothelial cells and their supporting glial and neuronal elements constitute a neurovascular unit (NVU). Blast injury disrupts gliovascular and neurovascular connections in addition to damaging endothelial cells, basal laminae, smooth muscle cells, and pericytes as well as causing extracellular matrix reorganization. Perivascular pathology becomes associated with phospho-tau accumulation and chronic perivascular inflammation. Disruption of the NVU should impact activity-dependent regulation of cerebral blood flow, blood-brain barrier permeability, and glymphatic flow. Here, we review work in an animal model of low-level blast injury that we have been studying for over a decade. We review work supporting the NVU as a locus of low-level blast injury. We integrate our findings with those from other laboratories studying similar models that collectively suggest that damage to astrocytes and other perivascular cells as well as chronic immune activation play a role in the persistent neurobehavioral changes that follow blast injury.
MeSH term(s)	Animals ; Humans ; Blast Injuries ; Endothelial Cells ; Brain Concussion ; Vascular System Injuries ; Astrocytes ; Inflammation
Language	English
Publishing date	2024-01-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25021150
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Article ; Online: Exposure to Low-Intensity Blast Increases Clearance of Brain Amyloid Beta.

Abutarboush, Rania / Reed, Eileen / Chen, Ye / Gu, Ming / Watson, Cameron / Kawoos, Usmah / Statz, Jonathan K / Tschiffely, Anna E / Ciarlone, Stephanie / Perez-Garcia, Georgina / Gama Sosa, Miguel A / de Gasperi, Rita / Stone, James R / Elder, Gregory A / Ahlers, Stephen T

Journal of neurotrauma

2024 Volume 41, Issue 5-6, Page(s) 685–704

Abstract: The long-term effects of exposure to blast overpressure are an important health concern in military personnel. Increase in amyloid beta (Aβ) has been documented after non-blast traumatic brain injury (TBI) and may contribute to neuropathology and an ... ...

Abstract	The long-term effects of exposure to blast overpressure are an important health concern in military personnel. Increase in amyloid beta (Aβ) has been documented after non-blast traumatic brain injury (TBI) and may contribute to neuropathology and an increased risk for Alzheimer's disease. We have shown that Aβ levels decrease following exposure to a low-intensity blast overpressure event. To further explore this observation, we examined the effects of a single 37 kPa (5.4 psi) blast exposure on brain Aβ levels, production, and clearance mechanisms in the acute (24 h) and delayed (28 days) phases post-blast exposure in an experimental rat model. Aβ and, notably, the highly neurotoxic detergent soluble Aβ42 form, was reduced at 24 h but not 28 days after blast exposure. This reduction was not associated with changes in the levels of Aβ oligomers, expression levels of amyloid precursor protein (APP), or increase in enzymes involved in the amyloidogenic cleavage of APP, the β- and ϒ-secretases BACE1 and presenilin-1, respectively. The levels of ADAM17 α-secretase (also known as tumor necrosis factor α-converting enzyme) decreased, concomitant with the reduction in brain Aβ. Additionally, significant increases in brain levels of the endothelial transporter, low-density related protein 1 (LRP1), and enhancement in co-localization of aquaporin-4 (AQP4) to perivascular astrocytic end-feet were observed 24 h after blast exposure. These findings suggest that exposure to low-intensity blast may enhance endothelial clearance of Aβ by LRP1-mediated transcytosis and alter AQP4-aided glymphatic clearance. Collectively, the data demonstrate that low-intensity blast alters enzymatic, transvascular, and perivascular clearance of Aβ.
MeSH term(s)	Animals ; Rats ; Amyloid beta-Peptides ; Amyloid Precursor Protein Secretases ; Aspartic Acid Endopeptidases ; Brain ; Amyloid beta-Protein Precursor ; Aquaporin 4
Chemical Substances	Amyloid beta-Peptides ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; Amyloid beta-Protein Precursor ; Aquaporin 4
Language	English
Publishing date	2024-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2023.0284
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Article ; Online: BCI-838, an orally active mGluR2/3 receptor antagonist pro-drug, rescues learning behavior deficits in the PS19 MAPT

Perez-Garcia, Georgina / Bicak, Mesude / Haure-Mirande, Jean-Vianney / Perez, Gissel M / Otero-Pagan, Alena / Gama Sosa, Miguel A / De Gasperi, Rita / Sano, Mary / Barlow, Carrolee / Gage, Fred H / Readhead, Benjamin / Ehrlich, Michelle E / Gandy, Sam / Elder, Gregory A

Neuroscience letters

2023 Volume 797, Page(s) 137080

Abstract: Tauopathies are a heterogeneous group of neurodegenerative disorders that are clinically and pathologically distinct from Alzheimer's disease (AD) having tau inclusions in neurons and/or glia as their most prominent neuropathological feature. BCI-838 ( ... ...

Abstract	Tauopathies are a heterogeneous group of neurodegenerative disorders that are clinically and pathologically distinct from Alzheimer's disease (AD) having tau inclusions in neurons and/or glia as their most prominent neuropathological feature. BCI-838 (MGS00210) is a group II metabotropic glutamate receptor (mGluR2/3) antagonist pro-drug. Previously, we reported that orally administered BCI-838 improved learning behavior and reduced anxiety in Dutch (APP
MeSH term(s)	Male ; Mice ; Humans ; Animals ; Prodrugs/therapeutic use ; Tauopathies/pathology ; tau Proteins/genetics ; Receptors, Metabotropic Glutamate ; Alzheimer Disease/pathology ; Mice, Transgenic ; Disease Models, Animal
Chemical Substances	BCI-838 ; metabotropic glutamate receptor 2 ; Prodrugs ; tau Proteins ; Receptors, Metabotropic Glutamate ; MAPT protein, human ; Mapt protein, mouse
Language	English
Publishing date	2023-01-16
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2023.137080
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Article ; Online: Hemovasculogenic origin of blood vessels in the developing mouse brain.

Gama Sosa, Miguel A / De Gasperi, Rita / Perez, Gissel M / Hof, Patrick R / Elder, Gregory A

The Journal of comparative neurology

2020 Volume 529, Issue 2, Page(s) 340–366

Abstract: Vascular structures in the developing brain are thought to form via angiogenesis from preformed blood vessels in the cephalic mesenchyme. Immunohistochemical studies of developing mouse brain from E10.5 to E13.5 revealed the presence of avascular blood ... ...

Abstract	Vascular structures in the developing brain are thought to form via angiogenesis from preformed blood vessels in the cephalic mesenchyme. Immunohistochemical studies of developing mouse brain from E10.5 to E13.5 revealed the presence of avascular blood islands of primitive erythroid cells expressing hemangioblast markers (Flk1, Tal1/Scl1, platelet endothelial cell adhesion molecule 1, vascular endothelial-cadherin, and CD34) and an endothelial marker recognized by Griffonia simplicifolia isolectin B4 (IB4) in the cephalic mesenchyme. These cells formed a perineural vascular plexus from which angiogenic sprouts originated and penetrated the neuroepithelium. In addition, avascular isolated cells expressing primitive erythroid, hemangioblast and endothelial makers were visible in the neuroepithelium where they generated vasculogenic and hemogenic foci. From E10.5 to E13.5, these vasculogenic foci were a source of new blood vessel formation in the developing brain. In vitro, cultured E13.5 brain endothelial cells contained hemogenic endothelial cells capable of generating erythroid cells. Similar cells were present in primary cultures of dissociated cells from E10.5 embryonic head. Our results provide new evidence that the brain vasculature, like that of the yolk sac and the eye choriocapillaris and hyaloid vascular systems, develops at least in part via hemovasculogenesis, a process in which vasculogenesis and hematopoiesis occur simultaneously.
MeSH term(s)	Animals ; Brain/blood supply ; Brain/cytology ; Brain/embryology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/embryology ; Female ; Mice ; Morphogenesis/physiology ; Pregnancy ; Yolk Sac/blood supply ; Yolk Sac/cytology ; Yolk Sac/embryology
Language	English
Publishing date	2020-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3086-7
ISSN	1096-9861 ; 0021-9967 ; 0092-7317
ISSN (online)	1096-9861
ISSN	0021-9967 ; 0092-7317
DOI	10.1002/cne.24951
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Article ; Online: (2R,6R)-Hydroxynorketamine Treatment of Rats Exposed to Repetitive Low-Level Blast Injury.

Garcia, Georgina Perez / Perez, Gissel M / Gasperi, Rita De / Sosa, Miguel A Gama / Otero-Pagan, Alena / Abutarboush, Rania / Kawoos, Usmah / Statz, Jonathan K / Patterson, Jacob / Zhu, Carolyn W / Hof, Patrick R / Cook, David G / Ahlers, Stephen T / Elder, Gregory A

Neurotrauma reports

2023 Volume 4, Issue 1, Page(s) 197–217

Abstract: Many military veterans who experienced blast-related traumatic brain injuries (TBIs) in the conflicts in Iraq and Afghanistan suffer from chronic cognitive and mental health problems, including post-traumatic stress disorder (PTSD). Male rats subjected ... ...

Abstract	Many military veterans who experienced blast-related traumatic brain injuries (TBIs) in the conflicts in Iraq and Afghanistan suffer from chronic cognitive and mental health problems, including post-traumatic stress disorder (PTSD). Male rats subjected to repetitive low-level blast exposure develop chronic cognitive and PTSD-related traits that develop in a delayed manner. Ketamine has received attention as a treatment for refractory depression and PTSD. (2R,6R)-hydroxynorketamine [(2R,6R)-HNK] is a ketamine metabolite that exerts rapid antidepressant actions. (2R,6R)-HNK has become of clinical interest because of its favorable side-effect profile, low abuse potential, and oral route of administration. We treated three cohorts of blast-exposed rats with (2R,6R)-HNK, beginning 7-11 months after blast exposure, a time when the behavioral phenotype is established. Each cohort consisted of groups (
Language	English
Publishing date	2023-03-30
Publishing country	United States
Document type	Journal Article
ISSN	2689-288X
ISSN (online)	2689-288X
DOI	10.1089/neur.2022.0088
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Article ; Online: Metabotropic Glutamate Receptor 2 Expression Is Chronically Elevated in Male Rats With Post-Traumatic Stress Disorder Related Behavioral Traits Following Repetitive Low-Level Blast Exposure.

De Gasperi, Rita / Gama Sosa, Miguel A / Perez Garcia, Georgina / Perez, Gissel M / Pryor, Dylan / Morrison, Chenel L-A / Lind, Rachel / Abutarboush, Rania / Kawoos, Usmah / Statz, Jonathan K / Patterson, Jacob / Hof, Patrick R / Zhu, Carolyn W / Ahlers, Stephen T / Cook, David G / Elder, Gregory A

Journal of neurotrauma

2023 Volume 41, Issue 5-6, Page(s) 714–733

Abstract: Many military veterans who experienced blast-related traumatic brain injuries in the conflicts in Iraq and Afghanistan currently suffer from chronic cognitive and mental health problems that include depression and post-traumatic stress disorder (PTSD). ... ...

Abstract	Many military veterans who experienced blast-related traumatic brain injuries in the conflicts in Iraq and Afghanistan currently suffer from chronic cognitive and mental health problems that include depression and post-traumatic stress disorder (PTSD). Male rats exposed to repetitive low-level blast develop cognitive and PTSD-related behavioral traits that are present for more than 1 year after exposure. We previously reported that a group II metabotropic receptor (mGluR2/3) antagonist reversed blast-induced behavioral traits. In this report, we explored mGluR2/3 expression following blast exposure in male rats. Western blotting revealed that mGluR2 protein (but not mGluR3) was increased in all brain regions studied (anterior cortex, hippocampus, and amygdala) at 43 or 52 weeks after blast exposure but not at 2 weeks or 6 weeks. mGluR2 RNA was elevated at 52 weeks while mGluR3 was not. Immunohistochemical staining revealed no changes in the principally presynaptic localization of mGluR2 by blast exposure. Administering the mGluR2/3 antagonist LY341495 after behavioral traits had emerged rapidly reversed blast-induced effects on novel object recognition and cued fear responses 10 months following blast exposure. These studies support alterations in mGluR2 receptors as a key pathophysiological event following blast exposure and provide further support for group II metabotropic receptors as therapeutic targets in the neurobehavioral effects that follow blast injury.
MeSH term(s)	Male ; Animals ; Rats ; Stress Disorders, Post-Traumatic ; Anxiety ; Blast Injuries/complications ; Amygdala ; Receptors, Metabotropic Glutamate
Chemical Substances	metabotropic glutamate receptor 2 ; Receptors, Metabotropic Glutamate
Language	English
Publishing date	2023-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2023.0252
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Article ; Online: Late chronic local inflammation, synaptic alterations, vascular remodeling and arteriovenous malformations in the brains of male rats exposed to repetitive low-level blast overpressures.

Gama Sosa, Miguel A / De Gasperi, Rita / Pryor, Dylan / Perez Garcia, Georgina S / Perez, Gissel M / Abutarboush, Rania / Kawoos, Usmah / Hogg, Seth / Ache, Benjamin / Sowa, Allison / Tetreault, Timothy / Varghese, Merina / Cook, David G / Zhu, Carolyn W / Tappan, Susan J / Janssen, William G M / Hof, Patrick R / Ahlers, Stephen T / Elder, Gregory A

Acta neuropathologica communications

2023 Volume 11, Issue 1, Page(s) 81

Abstract: In the course of military operations in modern war theaters, blast exposures are associated with the development of a variety of mental health disorders associated with a post-traumatic stress disorder-related features, including anxiety, impulsivity, ... ...

Abstract	In the course of military operations in modern war theaters, blast exposures are associated with the development of a variety of mental health disorders associated with a post-traumatic stress disorder-related features, including anxiety, impulsivity, insomnia, suicidality, depression, and cognitive decline. Several lines of evidence indicate that acute and chronic cerebral vascular alterations are involved in the development of these blast-induced neuropsychiatric changes. In the present study, we investigated late occurring neuropathological events associated with cerebrovascular alterations in a rat model of repetitive low-level blast-exposures (3 × 74.5 kPa). The observed events included hippocampal hypoperfusion associated with late-onset inflammation, vascular extracellular matrix degeneration, synaptic structural changes and neuronal loss. We also demonstrate that arteriovenous malformations in exposed animals are a direct consequence of blast-induced tissue tears. Overall, our results further identify the cerebral vasculature as a main target for blast-induced damage and support the urgent need to develop early therapeutic approaches for the prevention of blast-induced late-onset neurovascular degenerative processes.
MeSH term(s)	Rats ; Male ; Animals ; Vascular Remodeling ; Blast Injuries/complications ; Blast Injuries/pathology ; Brain/pathology ; Inflammation/pathology ; Arteriovenous Malformations/complications ; Arteriovenous Malformations/pathology ; Disease Models, Animal
Language	English
Publishing date	2023-05-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01553-6
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Article ; Online: Multimodal Assessment of Bottlenose Dolphin Auditory Nuclei Using 7-Tesla MRI, Immunohistochemistry and Stereology.

Orekhova, Ksenia / Selmanovic, Enna / De Gasperi, Rita / Gama Sosa, Miguel A / Wicinski, Bridget / Maloney, Brigid / Seifert, Alan / Alipour, Akbar / Balchandani, Priti / Gerussi, Tommaso / Graïc, Jean-Marie / Centelleghe, Cinzia / Di Guardo, Giovanni / Mazzariol, Sandro / Hof, Patrick R

Veterinary sciences

2022 Volume 9, Issue 12

Abstract: The importance of assessing neurochemical processes in the cetacean brain as a tool for monitoring their cognitive health and to indirectly model human neurodegenerative conditions is increasingly evident, although available data are largely ... ...

Abstract	The importance of assessing neurochemical processes in the cetacean brain as a tool for monitoring their cognitive health and to indirectly model human neurodegenerative conditions is increasingly evident, although available data are largely semiquantitative. High-resolution MRI for post-mortem brains and stereology allow for quantitative assessments of the cetacean brain. In this study, we scanned two brains of bottlenose dolphins in a 7-Tesla (7T) MR scanner and assessed the connectivity of the inferior colliculi and ventral cochlear nuclei using diffusion tensor imaging (DTI). Serial thick sections were investigated stereologically in one of the dolphins to generate rigorous quantitative estimates of identifiable cell types according to their morphology and expression of molecular markers, yielding reliable cell counts with most coefficients of error <10%. Fibronectin immunoreactivity in the dolphin resembled the pattern in a human chronic traumatic encephalopathy brain, suggesting that neurochemical compensation for insults such as hypoxia may constitute a noxious response in humans, while being physiological in dolphins. These data contribute to a growing body of knowledge on the morphological and neurochemical properties of the dolphin brain and highlight a stereological and neuroimaging workflow that may enable quantitative and translational assessment of pathological processes in the dolphin brain in the future.
Language	English
Publishing date	2022-12-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2768971-2
ISSN	2306-7381 ; 2306-7381
ISSN (online)	2306-7381
ISSN	2306-7381
DOI	10.3390/vetsci9120692
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Article ; Online: Unconventional animal models for traumatic brain injury and chronic traumatic encephalopathy.

Ackermans, Nicole L / Varghese, Merina / Wicinski, Bridget / Torres, Joshua / De Gasperi, Rita / Pryor, Dylan / Elder, Gregory A / Gama Sosa, Miguel A / Reidenberg, Joy S / Williams, Terrie M / Hof, Patrick R

Journal of neuroscience research

2021 Volume 99, Issue 10, Page(s) 2463–2477

Abstract: Traumatic brain injury (TBI) is one of the main causes of death worldwide. It is a complex injury that influences cellular physiology, causes neuronal cell death, and affects molecular pathways in the brain. This in turn can result in sensory, motor, and ...

Abstract	Traumatic brain injury (TBI) is one of the main causes of death worldwide. It is a complex injury that influences cellular physiology, causes neuronal cell death, and affects molecular pathways in the brain. This in turn can result in sensory, motor, and behavioral alterations that deeply impact the quality of life. Repetitive mild TBI can progress into chronic traumatic encephalopathy (CTE), a neurodegenerative condition linked to severe behavioral changes. While current animal models of TBI and CTE such as rodents, are useful to explore affected pathways, clinical findings therein have rarely translated into clinical applications, possibly because of the many morphofunctional differences between the model animals and humans. It is therefore important to complement these studies with alternative animal models that may better replicate the individuality of human TBI. Comparative studies in animals with naturally evolved brain protection such as bighorn sheep, woodpeckers, and whales, may provide preventive applications in humans. The advantages of an in-depth study of these unconventional animals are threefold. First, to increase knowledge of the often-understudied species in question; second, to improve common animal models based on the study of their extreme counterparts; and finally, to tap into a source of biological inspiration for comparative studies and translational applications in humans.
MeSH term(s)	Animals ; Birds ; Brain/anatomy & histology ; Brain/pathology ; Brain Injuries, Traumatic/genetics ; Brain Injuries, Traumatic/pathology ; Caenorhabditis elegans ; Cetacea ; Chronic Traumatic Encephalopathy/genetics ; Chronic Traumatic Encephalopathy/pathology ; Disease Models, Animal ; Drosophila ; Humans ; Mice ; Rats ; Sheep ; Swine
Language	English
Publishing date	2021-07-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.24920
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Article ; Online: Progressive Transcriptional Changes in the Amygdala Implicate Neuroinflammation in the Effects of Repetitive Low-Level Blast Exposure in Male Rats.

De Gasperi, Rita / Gama Sosa, Miguel A / Perez Garcia, Georgina S / Perez, Gissel M / Abutarboush, Rania / Kawoos, Usmah / Statz, Jonathan K / Patterson, Jacob / Hof, Patrick R / Katsel, Pavel / Cook, David G / Ahlers, Stephen T / Elder, Gregory A

Journal of neurotrauma

2022 Volume 40, Issue 5-6, Page(s) 561–577

Abstract: Chronic mental health problems are common among military veterans who sustained blast-related traumatic brain injuries. The reasons for this association remain unexplained. Male rats exposed to repetitive low-level blast overpressure (BOP) exposures ... ...

Abstract	Chronic mental health problems are common among military veterans who sustained blast-related traumatic brain injuries. The reasons for this association remain unexplained. Male rats exposed to repetitive low-level blast overpressure (BOP) exposures exhibit chronic cognitive and post-traumatic stress disorder (PTSD)-related traits that develop in a delayed fashion. We examined blast-induced alterations on the transcriptome in four brain areas (anterior cortex, hippocampus, amygdala, and cerebellum) across the time frame over which the PTSD-related behavioral phenotype develops. When analyzed at 6 weeks or 12 months after blast exposure, relatively few differentially expressed genes (DEGs) were found. However, longitudinal analysis of amygdala, hippocampus, and anterior cortex between 6 weeks and 12 months revealed blast-specific DEG patterns. Six DEGs (hyaluronan and proteoglycan link protein 1 [Hapln1], glutamate metabotropic receptor 2 [Grm2], purinergic receptor P2y12 [P2ry12], C-C chemokine receptor type 5 [Ccr5], phenazine biosynthesis-like protein domain containing 1 [Pbld1], and cadherin related 23 [Cdh23]) were found altered in all three brain regions in blast-exposed animals. Pathway enrichment analysis using all DEGs or those uniquely changed revealed different transcription patterns in blast versus sham. In particular, the amygdala in blast-exposed animals had a unique set of enriched pathways related to stress responses, oxidative phosphorylation, and mitochondrial dysfunction. Upstream analysis implicated tumor necrosis factor (TNF)α signaling in blast-related effects in amygdala and anterior cortex. Eukaryotic initiating factor eIF4E (EIF4e), an upstream regulator of P2ry12 and Ccr5, was predicted to be activated in the amygdala. Quantitative polymerase chain reaction (qPCR) validated longitudinal changes in two TNFα regulated genes (cathepsin B [Ctsb], Hapln1), P2ry12, and Grm2. These studies have implications for understanding how blast injury damages the brain and implicates inflammation as a potential therapeutic target.
MeSH term(s)	Rats ; Male ; Animals ; Neuroinflammatory Diseases ; Eukaryotic Initiation Factor-4E/metabolism ; Explosions ; Brain Injuries, Traumatic/metabolism ; Blast Injuries/pathology ; Amygdala/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Eukaryotic Initiation Factor-4E ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2022-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2022.0282
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