To study the potential causal role of CCR5 in cognitive deficits in AD, we injected soluble Aβ1-42 or a control (Aβ42-1) oligomers in the dorsal CA1 region of the hippocampus and found that Aβ1-42 injection resulted in severe memory impairment in the object place recognition (OPR) and novel object recognition (NOR) tests. Aβ1-42 injection caused an increase in Ccr5, Ccl3, and Ccl4 in the dorsal hippocampus, and the expression levels of CCR5 and its ligands remained elevated at 2 weeks after Aβ1-42 injection. Knocking down Ccr5 in the CA1 region of dorsal hippocampus reversed the increase in microglia number and size in dorsal CA1 and rescued memory deficits. These results indicate that CCR5 plays an important role in modulating Aβ1-42-induced learning and memory deficits, and suggest that CCR5 antagonists may serve as a potential treatment to improve cognitive deficits associated with AD.
https://www.sciencedirect.com/science/article...2724000017

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