Show simple item record Laskowitz, DT Song, P Wang, H Mace, B Sullivan, PM Vitek, MP Dawson, HN
dc.coverage.spatial United States 2011-04-15T16:46:33Z 2010-11
dc.identifier.citation J Neurotrauma, 2010, 27 (11), pp. 1983 - 1995
dc.description.abstract Cognitive impairment is common following traumatic brain injury (TBI), and neuroinflammatory mechanisms may predispose to the development of neurodegenerative disease. Apolipoprotein E (apoE) polymorphisms modify neuroinflammatory responses, and influence both outcome from acute brain injury and the risk of developing neurodegenerative disease. We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele. The administration of an apoE-mimetic peptide markedly reduced the development of neurodegenerative pathology in mice homozygous for apoE3 as well as apoE3/E4 heterozygotes. These results demonstrate that TBI accelerates the cardinal neuropathological features of neurodegenerative disease, and establishes the potential for apoE mimetic therapies in reducing pathology associated with neurodegeneration.
dc.format.extent 1983 - 1995
dc.language eng
dc.language.iso en_US en_US
dc.relation.ispartof J Neurotrauma
dc.relation.isversionof 10.1089/neu.2010.1396
dc.subject Amyloid beta-Peptides
dc.subject Animals
dc.subject Apolipoproteins E
dc.subject Blotting, Western
dc.subject Brain
dc.subject Brain Injuries
dc.subject Cytokines
dc.subject Enzyme-Linked Immunosorbent Assay
dc.subject Genetic Therapy
dc.subject Gliosis
dc.subject Humans
dc.subject Immunohistochemistry
dc.subject Male
dc.subject Mice
dc.subject Mice, Transgenic
dc.subject Motor Activity
dc.subject Neurodegenerative Diseases
dc.subject Platelet-Derived Growth Factor
dc.subject Polymorphism, Genetic
dc.subject Psychomotor Performance
dc.subject RNA, Messenger
dc.subject Tumor Necrosis Factor-alpha
dc.subject tau Proteins
dc.title Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic.
dc.type Journal Article
dc.description.version Version of Record en_US 2010-11-0 en_US
duke.description.endpage 1995 en_US
duke.description.issue 11 en_US
duke.description.startpage 1983 en_US
duke.description.volume 27 en_US
dc.relation.journal Journal of neurotrauma en_US
pubs.issue 11
pubs.organisational-group /Duke
pubs.organisational-group /Duke/Institutes and Provost's Academic Units
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers/Global Health Institute
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Neurobiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Anesthesiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Geriatrics
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Neurology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Neurology/Neurology, Behavioral Neurology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Neurology/Neurology, Neurocritical Care
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Clinical Research Institute
pubs.publication-status Published
pubs.volume 27
dc.identifier.eissn 1557-9042

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