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Medientyp:
E-Artikel
Titel:
HIV encephalopathy: glial activation and hippocampal neuronal apoptosis, but limited neural repair
Beteiligte:
Tauber, SC;
Staszewski, O;
Prinz, M;
Weis, J;
Nolte, K;
Bunkowski, S;
Brück, W;
Nau, R
Erschienen:
Wiley, 2016
Erschienen in:HIV Medicine
Sprache:
Englisch
DOI:
10.1111/hiv.12288
ISSN:
1464-2662;
1468-1293
Entstehung:
Anmerkungen:
Beschreibung:
<jats:sec><jats:title>Objectives</jats:title><jats:p><jats:styled-content style="fixed-case">HIV</jats:styled-content> infection affects the central nervous system (<jats:styled-content style="fixed-case">CNS</jats:styled-content>), frequently causing cognitive impairment. Hippocampal injury impedes the ability to transfer information into memory. Therefore, we aimed to examine neuronal injury and repair in the hippocampal formation in <jats:styled-content style="fixed-case">HIV</jats:styled-content> encephalopathy.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We compared neuropathological findings in 14 autopsy cases after death from systemic complications of <jats:styled-content style="fixed-case">HIV</jats:styled-content> infection and in 15 age‐matched <jats:styled-content style="fixed-case">HIV</jats:styled-content>‐negative control cases after sudden death from nonneurological causes using immunohistochemistry.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The density of apoptotic granule cells in the dentate gyrus was higher in <jats:styled-content style="fixed-case">HIV</jats:styled-content>‐infected than in control cases (<jats:italic>P</jats:italic> = 0.048). Proliferation of neural progenitor cells in the dentate gyrus was increased in <jats:styled-content style="fixed-case">HIV</jats:styled-content> infection (<jats:italic>P</jats:italic> = 0.028), whereas the density of recently generated <jats:styled-content style="fixed-case">TUC</jats:styled-content>‐4 [TOAD (turned on after division)/Ulip/CRMP family 4]‐expressing neurons in this region was not significantly elevated in <jats:styled-content style="fixed-case">HIV</jats:styled-content>‐infected cases (<jats:italic>P</jats:italic> = 0.13). <jats:styled-content style="fixed-case">HIV</jats:styled-content> infection caused microglial activation and astrocytosis in the neocortex and hippocampal formation. Conversely, we were unable to detect more pronounced axonal injury in <jats:styled-content style="fixed-case">HIV</jats:styled-content>‐infected than in control cases.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>As in other infections involving the <jats:styled-content style="fixed-case">CNS</jats:styled-content>, apoptosis of hippocampal neurons accompanied by microglial activation and astrocytosis is a prominent feature of <jats:styled-content style="fixed-case">HIV</jats:styled-content> encephalopathy. The regenerative potential, assessed using the density of young neurons in the hippocampal dentate gyrus, in <jats:styled-content style="fixed-case">HIV</jats:styled-content> infection appears to be lower than in acute bacterial meningitis and septic encephalitis.</jats:p></jats:sec>