Neuroinflammation and Cognitive Impairment in HIV-1 Transgenic Rats
Author Information
Author(s): Rao Jagadeesh Sridhara, Kim Hyung-Wook, Kellom Matthew, Greenstein Dede, Chen Mei, Kraft Andrew David, Harry Gaylia Jean, Rapoport Stanley Isaac, Basselin Mireille
Primary Institution: National Institute on Aging, Bethesda, MD, USA
Hypothesis
HIV-1 Tg rats would show upregulated brain inflammatory and arachidonic acid cascade markers and a deficit of synaptic proteins.
Conclusion
HIV-1 Tg rats show elevated brain markers of neuroinflammation and arachidonic acid metabolism, with a deficit in several synaptic proteins, which may contribute to cognitive impairment.
Supporting Evidence
- HIV-1 Tg rat brain showed significantly higher levels of inflammatory cytokines IL-1β and TNFα.
- CD11b, a marker for activated microglia, was elevated significantly in HIV-1 Tg rats.
- Brain-derived neurotrophic factor (BDNF) and drebrin levels were significantly decreased in HIV-1 Tg rats.
Takeaway
The study found that rats with HIV-1 have more inflammation in their brains and fewer proteins that help with brain connections, which might make it harder for them to think.
Methodology
The study measured protein and mRNA levels of neuroinflammation and arachidonic acid cascade markers in the brains of HIV-1 Tg and control rats.
Limitations
The study's findings may be influenced by the small sample size and potential contamination of brain tissue by peripheral cells.
Participant Demographics
7- to 9-month-old male Fischer 344/Hsd HIV-1 Tg rats and age-matched parental wild-type Fischer 344/Hsd non-Tg control rats.
Statistical Information
P-Value
p<0.001 for IL-1β and p<0.01 for TNFα
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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