Human CNS cultures exposed to HIV-1 gp120 reproduce dendritic injuries of HIV-1-associated dementia
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BioMed Central
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Human CNS cultures exposed to HIV-1 gp120 reproduce dendritic injuries of HIV-1-associated dementia Sam Iskander1, Kimberley A Walsh1 and Robert R Hammond*1,2 Address: 1Department of Pathology, London Health Sciences Centre, University of Western Ontario, London, ON, Canada and 2Department of Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario, London, ON, Canada Email: Sam Iskander - [email protected]; Kimberley A Walsh - [email protected]; Robert R Hammond* - [email protected] * Corresponding author
Published: 27 May 2004 Journal of Neuroinflammation 2004, 1:7
Received: 08 April 2004 Accepted: 27 May 2004
This article is available from: http://www.jneuroinflammation.com/content/1/1/7 © 2004 Iskander et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
Abstract HIV-1-associated dementia remains a common subacute to chronic central nervous system degeneration in adult and pediatric HIV-1 infected populations. A number of viral and host factors have been implicated including the HIV-1 120 kDa envelope glycoprotein (gp120). In human postmortem studies using confocal scanning laser microscopy for microtubule-associated protein 2 and synaptophysin, neuronal dendritic pathology correlated with dementia. In the present study, primary human CNS cultures exposed to HIV-1 gp120 at 4 weeks in vitro suffered gliosis and dendritic damage analogous to that described in association with HIV-1-associated dementia.
Introduction HIV-1-associated dementia (HAD) is a late, subacute to chronic dementia characterized by a progressive and severe decline in cognitive and motor function. HAD remains a major debilitating consequence of HIV-1 infection. It is an independent risk factor for death from AIDS and the most common form of dementia in young adults worldwide [1-5]. Evidence of a reduction in the incidence of HAD [6,7] and reports of cognitive improvement in cases of mild dementia with highly active antiretroviral therapy (HAART) have been presented [8]. Other studies have failed to identify a lower incidence of HAD postHAART and a number of experts note the potential for a changing tempo of HAD from a precipitous dementia to one with a more protracted course and greater incidence in patients with relatively preserved CD4 counts [3,4,8]. It is premature to accurately predict how HAART will affect the incidence of HAD in the long term. HAART clearly does not afford complete protection and the potential for an increase in the prevalence of HAD has been raised by many [2,3,6,8-11].
HIV-1 associated neuronal damage has been characterized with evidence for both cytocidal and subcytocidal injuries. Evidence of loss of large neurons in the orbitofrontal, temporal and parietal regions [12] has been demonstrated in association with HAD. Other investigations have fai
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