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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1999-7-26
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pubmed:abstractText |
Progressive neuronal degeneration in brain regions involved in learning and memory processes is a common occurrence in patients infected with human immunodeficiency virus type 1 (HIV-1). We now report that levels of Par-4, a protein recently linked to neuronal apoptosis in Alzheimer's disease, are increased in neurons in hippocampus of human patients with HIV encephalitis and in monkeys infected with a chimeric strain of HIV-1 and simian immunodeficiency virus. Par-4 levels increased rapidly in cultured hippocampal neurons following exposure to the neurotoxic HIV-1 protein Tat, and treatment of the cultures with a Par-4 antisense oligonucleotide protected the neurons against Tat-induced apoptosis. Additional findings show that Par-4 participates at an early stage of Tat-induced neuronal apoptosis before caspase activation, oxidative stress, and mitochondrial dysfunction. Our data suggest that Par-4 may be a mediator of neuronal apoptosis in HIV encephalitis and that therapeutic approaches targeting the Par-4 apoptotic cascade may prove beneficial in preventing neuronal degeneration and associated dementia in patients infected with HIV-1.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-1303631,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-1538584,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-1676893,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-1909852,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-2360420,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-2845276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-7695237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8005510,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8097316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8495704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8498818,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8498837,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8627665,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8787150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8828741,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8903316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-8943206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9111179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9199316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9217970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9223134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9229134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9335256,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9342064,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9354812,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9422341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9460791,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9476001,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9501225,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9701251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9743565,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10393834-9878167
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
155
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
39-46
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10393834-Animals,
pubmed-meshheading:10393834-Apoptosis,
pubmed-meshheading:10393834-Apoptosis Regulatory Proteins,
pubmed-meshheading:10393834-Carrier Proteins,
pubmed-meshheading:10393834-Cells, Cultured,
pubmed-meshheading:10393834-Chimera,
pubmed-meshheading:10393834-Encephalitis,
pubmed-meshheading:10393834-Gene Products, tat,
pubmed-meshheading:10393834-HIV,
pubmed-meshheading:10393834-HIV Infections,
pubmed-meshheading:10393834-Hippocampus,
pubmed-meshheading:10393834-Humans,
pubmed-meshheading:10393834-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:10393834-Macaca mulatta,
pubmed-meshheading:10393834-Neurons,
pubmed-meshheading:10393834-Oligonucleotides, Antisense,
pubmed-meshheading:10393834-Rats,
pubmed-meshheading:10393834-Rats, Sprague-Dawley,
pubmed-meshheading:10393834-Simian Acquired Immunodeficiency Syndrome,
pubmed-meshheading:10393834-tat Gene Products, Human Immunodeficiency Virus
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pubmed:year |
1999
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pubmed:articleTitle |
Evidence that Par-4 participates in the pathogenesis of HIV encephalitis.
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pubmed:affiliation |
Sanders-Brown Research Center on Aging, Department of Neurology, Lexington, Kentucky, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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