Chemerin-9 Peptide Enhances Memory and Ameliorates Aβ₁₋₄₂-Induced Object Memory Impairment in Mice

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  • Lei ZeLin
    Key Laboratory of Biotherapy and Regenerative Medicine, the First Hospital of Lanzhou University
  • Lu YaQin
    Department of Neurology, the First Hospital of Lanzhou University
  • Bai Xue
    Key Laboratory of Biotherapy and Regenerative Medicine, the First Hospital of Lanzhou University
  • Jiang ZhenXiu
    Department of Neurology, the First Hospital of Lanzhou University
  • Yu Qin
    Key Laboratory of Biotherapy and Regenerative Medicine, the First Hospital of Lanzhou University

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  • Chemerin-9 Peptide Enhances Memory and Ameliorates Aβ<sub>1–42</sub>-Induced Object Memory Impairment in Mice

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<p>Accumulating evidence suggests that the inhibition of neuroinflammation is a potential target for therapeutic or preventive strategies for Alzheimer’s disease (AD). Chemerin has attracted particular attention for its role in the regulation of inflammation. In addition, amyloid β1–42 (Aβ1–42) can interact with chemokine-like receptor 1 (CMKLR1), the receptor for chemerin, and induce microglial chemotaxis. Meanwhile, CMKLR1 is expressed in the brain, and both chemerin and Aβ1–42 share the same receptor. Thus, we hypothesized that chemerin (C9), a chemerin-derived nonapeptide, may have the potential to ameliorate Aβ1–42 mediated AD disease progression. The results showed that an intracerebroventricular (i.c.v.) injection of C9 (8 µg/kg) facilitated memory formation and improved memory retention, as evidenced by the results of both the novel object recognition test (NOR) and object location recognition (OLR) tasks. These memory-enhancing effects of C9 were also observed after C9 (2 µg/kg) was infused into the hippocampus. Moreover, we found that treatment with C9 reversed the deficits in memory and learning ability induced by oligomeric Aβ1–42. Meanwhile, C9 also significantly inhibited Aβ1–42-induced increases in the levels of pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the hippocampus. The same results were obtained for Western blotting and enzyme-linked immunosorbent assay (ELISA) experiments. Finally, we observed that C9 did not affect locomotor activity, suggesting that its improvement of memory is not a false positive induced by hypolocomotion. In conclusion, C9 may facilitate memory formation, prolong memory retention, and ameliorate Aβ1–42-induced memory impairment, suggesting that C9 may potentially represent a novel strategy for the treatment of AD.</p>

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