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Intraneuronal ß-Amyloid Accumulation: Aging HIV-1 Human and HIV-1 Transgenic Rat Brain.
Li, Hailong; McLaurin, Kristen A; Mactutus, Charles F; Likins, Benjamin; Huang, Wenfei; Chang, Sulie L; Booze, Rosemarie M.
Afiliación
  • Li H; Department of Psychology, University of South Carolina, Columbia, SC 29208, USA.
  • McLaurin KA; Department of Psychology, University of South Carolina, Columbia, SC 29208, USA.
  • Mactutus CF; Department of Psychology, University of South Carolina, Columbia, SC 29208, USA.
  • Likins B; Department of Psychology, University of South Carolina, Columbia, SC 29208, USA.
  • Huang W; Institute of NeuroImmune Pharmacology, Seton Hall University, South Orange, NJ 07079, USA.
  • Chang SL; Department of Biological Sciences, Seton Hall University, South Orange, NJ 07079, USA.
  • Booze RM; Institute of NeuroImmune Pharmacology, Seton Hall University, South Orange, NJ 07079, USA.
Viruses ; 14(6)2022 06 10.
Article en En | MEDLINE | ID: mdl-35746739
The prevalence of HIV-1 associated neurocognitive disorders (HAND) is significantly greater in older, relative to younger, HIV-1 seropositive individuals; the neural pathogenesis of HAND in older HIV-1 seropositive individuals, however, remains elusive. To address this knowledge gap, abnormal protein aggregates (i.e., ß-amyloid) were investigated in the brains of aging (>12 months of age) HIV-1 transgenic (Tg) rats. In aging HIV-1 Tg rats, double immunohistochemistry staining revealed abnormal intraneuronal ß-amyloid accumulation in the prefrontal cortex (PFC) and hippocampus, relative to F344/N control rats. Notably, in HIV-1 Tg animals, increased ß-amyloid accumulation occurred in the absence of any genotypic changes in amyloid precursor protein (APP). Furthermore, no clear amyloid plaque deposition was observed in HIV-1 Tg animals. Critically, ß-amyloid was co-localized with neurons in the cortex and hippocampus, supporting a potential mechanism underlying synaptic dysfunction in the HIV-1 Tg rat. Consistent with these neuropathological findings, HIV-1 Tg rats exhibited prominent alterations in the progression of temporal processing relative to control animals; temporal processing relies, at least in part, on the integrity of the PFC and hippocampus. In addition, in post-mortem HIV-1 seropositive individuals with HAND, intraneuronal ß-amyloid accumulation was observed in the dorsolateral PFC and hippocampal dentate gyrus. Consistent with observations in the HIV-1 Tg rat, no amyloid plaques were found in these post-mortem HIV-1 seropositive individuals with HAND. Collectively, intraneuronal ß-amyloid aggregation observed in the PFC and hippocampus of HIV-1 Tg rats supports a potential factor underlying HIV-1 associated synaptodendritic damage. Further, the HIV-1 Tg rat provides a biological system to model HAND in older HIV-1 seropositive individuals.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: VIH-1 / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Aged / Animals / Humans Idioma: En Revista: Viruses Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: VIH-1 / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Aged / Animals / Humans Idioma: En Revista: Viruses Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza