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Text
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URL Address
<a href="http://doi.org/10.1089/neu.2015.3970" target="_blank" rel="noreferrer noopener">http://doi.org/10.1089/neu.2015.3970</a>
Pages
625–640
Issue
7
Volume
33
Dublin Core
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Title
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Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.
Publisher
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Journal of neurotrauma
Date
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2016
2016-04
Subject
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Alzheimer Disease/etiology/*metabolism/pathology; Alzheimer's disease; Amyloid beta-Peptides/*metabolism; Animal; Animal/physiology; Animals; Behavior; Blotting; Brain Injuries; Brain/*metabolism/pathology; Disease Models; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Humans; Immunohistochemistry; Inbred C57BL; Inflammation/*metabolism/pathology; macrophage; Mice; neuroinflammation; Transgenic; traumatic brain injury; Traumatic/complications/*metabolism/*pathology; Western
Creator
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Kokiko-Cochran Olga N; Ransohoff Lena; Veenstra Mike; Lee Sungho; Saber Maha; Sikora Matt; Teknipp Ryan; Xu Guixiang; Bemiller Shane M; Wilson Gina; Crish Samuel; Bhaskar Kiran; Lee Yu-Shang; Ransohoff Richard M; Lamb Bruce T
Description
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Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. The R1.40 mouse model of cerebral amyloidosis was used, with a focus on time points well before robust AD pathologies. Unexpectedly, in R1.40 mice, the acute neuroinflammatory response to TBI was strikingly muted, with reduced numbers of CNS myeloid cells acquiring a macrophage phenotype and decreased expression of inflammatory cytokines. At chronic time points, macrophage activation substantially declined in non-Tg TBI mice; however, it was relatively unchanged in R1.40 TBI mice. The persistent inflammatory response coincided with significant tissue loss between 3 and 120 days post-injury in R1.40 TBI mice, which was not observed in non-Tg TBI mice. Surprisingly, inflammatory cytokine expression was enhanced in R1.40 mice compared with non-Tg mice, regardless of injury group. Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator.
Identifier
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<a href="http://doi.org/10.1089/neu.2015.3970" target="_blank" rel="noreferrer noopener">10.1089/neu.2015.3970</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Alzheimer Disease/etiology/*metabolism/pathology
Alzheimer's disease
Amyloid beta-Peptides/*metabolism
Animal
Animal/physiology
Animals
Behavior
Bemiller Shane M
Bhaskar Kiran
Blotting
Brain Injuries
Brain/*metabolism/pathology
Crish Samuel
Department of Pharmaceutical Sciences
Disease Models
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Humans
Immunohistochemistry
Inbred C57BL
Inflammation/*metabolism/pathology
Journal of neurotrauma
Kokiko-Cochran Olga N
Lamb Bruce T
Lee Sungho
Lee Yu-Shang
macrophage
Mice
NEOMED College of Pharmacy
Neuroinflammation
Ransohoff Lena
Ransohoff Richard M
Saber Maha
Sikora Matt
Teknipp Ryan
Transgenic
Traumatic brain injury
Traumatic/complications/*metabolism/*pathology
Veenstra Mike
Western
Wilson Gina
Xu Guixiang