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Neuroprotective Activities of Sodium Valproate in a Murine Model of Human Immunodeficiency Virus-1 Encephalitis

Neuroprotective Activities of Sodium Valproate in a Murine Model of Human Immunodeficiency... 9162 • The Journal of Neuroscience, October 8, 2003 • 23(27):9162–9170 Cellular/Molecular Neuroprotective Activities of Sodium Valproate in a Murine Model of Human Immunodeficiency Virus-1 Encephalitis 1,2 1,2 1,2 1,2 1,2 5 Huanyu Dou, Kevin Birusingh, Jill Faraci, Santhi Gorantla, Larisa Y. Poluektova, Sanjay B. Maggirwar, 5 4,5 1,2,3 Stephen Dewhurst, Harris A. Gelbard, and Howard E. Gendelman 1 2 3 Center for Neurovirology and Neurodegenerative Disorders, Department of Pathology and Microbiology, and Department of Internal Medicine, 4 5 University of Nebraska Medical Center, Omaha, Nebraska 68198-5215, Center for Aging and Developmental Biology, and Department of Neurology, Pediatrics, and Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York 14642 Human immunodeficiency virus-1 (HIV-1) infection of the nervous system can result in neuroinflammatory events leading first to neuronal dysfunction then to cognitive and behavioral impairments in infected people. The multifaceted nature of the disease process, commonly called HIV-1-associated dementia (HAD), provides a number of adjunctive therapeutic opportunities. One proposed adjunc- tive therapy is sodium valproate (VPA), an anticonvulsant known to promote neurite outgrowth and increase -catenin through inhib- iting glycogen synthase kinase 3 activity and tau phosphorylation. We now show that VPA treatment of rat cortical neurons exposed http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Unpaywall

Neuroprotective Activities of Sodium Valproate in a Murine Model of Human Immunodeficiency Virus-1 Encephalitis

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Unpaywall
ISSN
0270-6474
DOI
10.1523/jneurosci.23-27-09162.2003
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Abstract

9162 • The Journal of Neuroscience, October 8, 2003 • 23(27):9162–9170 Cellular/Molecular Neuroprotective Activities of Sodium Valproate in a Murine Model of Human Immunodeficiency Virus-1 Encephalitis 1,2 1,2 1,2 1,2 1,2 5 Huanyu Dou, Kevin Birusingh, Jill Faraci, Santhi Gorantla, Larisa Y. Poluektova, Sanjay B. Maggirwar, 5 4,5 1,2,3 Stephen Dewhurst, Harris A. Gelbard, and Howard E. Gendelman 1 2 3 Center for Neurovirology and Neurodegenerative Disorders, Department of Pathology and Microbiology, and Department of Internal Medicine, 4 5 University of Nebraska Medical Center, Omaha, Nebraska 68198-5215, Center for Aging and Developmental Biology, and Department of Neurology, Pediatrics, and Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York 14642 Human immunodeficiency virus-1 (HIV-1) infection of the nervous system can result in neuroinflammatory events leading first to neuronal dysfunction then to cognitive and behavioral impairments in infected people. The multifaceted nature of the disease process, commonly called HIV-1-associated dementia (HAD), provides a number of adjunctive therapeutic opportunities. One proposed adjunc- tive therapy is sodium valproate (VPA), an anticonvulsant known to promote neurite outgrowth and increase -catenin through inhib- iting glycogen synthase kinase 3 activity and tau phosphorylation. We now show that VPA treatment of rat cortical neurons exposed

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Journal of Neuroscience – Unpaywall

Published: Oct 8, 2003

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