Persistent Hijacking of Brain Proteasomes in HIV-Associated Dementia

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dc.contributor Benjamin B . Gelman , MD , PhD
dc.contributor Miles W . Cloyd , PhD
dc.contributor David J . McAdoo , PhD
dc.contributor Claudio A . Soto , PhD
dc.contributor Dennis L . Kolson , MD , PhD
dc.creator Nguyen , Trung Phuoc
dc.date 2010 -09 -28
dc.date.accessioned 2011 -04 -27T21 :39 :51Z
dc.date.available 2011 -04 -27T21 :39 :51Z
dc.date.issued 2011 -04 -27T21 :39 :51Z
dc.identifier http : / /etd .utmb .edu /theses /available /etd -02202009 -130702 /
dc.identifier.uri http : / /hdl .handle .net /2249 .1 /35812
dc.description Human immunodeficiency virus -1 (HIV ) infection of the central nervous system results in a syndrome of neuropsychological impairment , motor deficits , and behavioral changes diagnosed as HIV -associated dementia . Findings of increased ubiquitin -stained deposits and high molecular weight ubiquitin -protein conjugates in brains of HIV -positive subjects suggest impaired protein turnover by the ubiquitin -proteasome system analogous to neurodegenerative disorders such as Alzheimers disease and Parkinsons disease . HIV infection of the brain and the consequent inflammatory response was hypothesized to alter the ubiquitin -proteasome system , leading to altered brain protein turnover and neuronal function . Investigations into the ubiquitin -proteasome system in HIV -infected brains were performed using the resources of the Texas NeuroAIDS Research Center and the National NeuroAIDS Tissue Consortium , including clinical data and frontal cortex brain tissue from 153 autopsy cases . Assessment of frontal cortex proteasome proteolytic activity revealed an abnormal catalytic profile that was more severe in those with HIV -associated neuropsychological impairment or HIV encephalitis . Proteasome subunit composition analysis by immunoblotting showed increases in immunoproteasome subunits LMP7 and PA28 alpha and decreases in constitutive proteasome regulatory subunit Rpn2 in the frontal cortex of HIV -positive subjects that correlated with the abnormal proteasome proteinase profile and were associated with neuropsychological impairment and HIV encephalitis . Immunoproteasome increases correlated with lower performance on neurocognitive tests specific for frontal lobe functioning domains , providing indications of regional specificity . Immunoproteasome increases also correlated with increases in frontal cortex tissue HIV loads . Immunoproteasomes were localized by immunofluorescence to the perikarya and distal processes of neurons , as well as to oligodendrocytes , astrocytes , and microglia . The potential consequence of immunoproteasomes in neurons was investigated with the analysis of synaptic proteins . Decreases in synaptophysin correlated with immunoproteasome increases , indicating the potential for synaptic protein alterations associated with immunoproteasomes . Analysis of isolated nerve endings , or synaptosomes , revealed immunoproteasome increases in synapses of HIV -positive subjects that correlated with increases in 14 -3 -3 zeta and decreases in synapsin 1 . These findings suggest hijacking of constitutive proteasomes by immunoproteasomes with the persistent inflammatory response in HIV -infected brains . Ubiquitin -mediated protein turnover by constitutive proteasomes is consequently impaired , resulting in the dysregulation of neuronal and synaptic protein composition that leads to neuronal dysfunction .
dc.format application /pdf
dc.language en
dc.publisher UTMB
dc.rights restricted
dc.rights I hereby certify that , if appropriate , I have obtained and attached hereto a written permission statement from the owner (s ) of each third party copyrighted matter to be included in my thesis , dissertation , or project report , allowing distribution as specified below . I certify that the version I submitted is the same as that approved by my advisory committee . I hereby grant to University of Texas Medical Branch or its agents the non -exclusive license to archive and make accessible , under the conditions specified below , my thesis , dissertation , or project report in whole or in part in all forms of media , now or hereafter known . I retain all other ownership rights to the copyright of the thesis , dissertation or project report . I also retain the right to use in future works (such as articles or books ) all or part of this thesis , dissertation , or project report .
dc.source http : / /etd .utmb .edu /theses /available /etd -02202009 -130702 /
dc.subject Neuroscience & Cell Biology
dc.title Persistent Hijacking of Brain Proteasomes in HIV -Associated Dementia
dc.type text

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Persistent Hijacking of Brain Proteasomes in HIV-Associated Dementia. Available electronically from http : / /hdl .handle .net /2249 .1 /35812 .

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