Cited by 23Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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

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Lei, ZeLin, Lu, YaQin, Bai, Xue, Jiang, ZhenXiu, Yu, Qin·2020·Biological and Pharmaceutical Bulletin

Abstract

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.

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Authors
Lei, Z., Lu, Y., Bai, X., Jiang, Z., & Yu, Q.
Affiliations
First Hospital of Lanzhou University (CN)
Venue
Biological and Pharmaceutical Bulletin
Published
2020-02-01
Volume
43
Issue
2
Pages
272-283
ISSN
  • 0918-6158 (ISSN-L)
  • 1347-5215
OpenAlex
W2987005177
Cited by
23
References
54
Citations by year
2026: 3 · 2025: 2 · 2024: 1 · 2023: 7 · 2022: 5 · 2021: 4 · 2020: 1
FWCI
1.71
Type
journal article
Language
en
Open access
Locations
  • Biological and Pharmaceutical Bulletin (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
chemerin, Alzheimer's disease, amyloid-beta 42, CMKLR1, memory enhancement, neuroinflammation, inflammatory cytokines, hippocampus, microglial chemotaxis, novel object recognition
MeSH terms
Alzheimer Disease, Animals, Hippocampus, Inflammation, Male, Memory Disorders, Motor Activity, Peptide Fragments, Cytokines, Amyloid beta-Peptides, Chemokines, Receptors, Chemokine, Recognition, Psychology, Intercellular Signaling Peptides and Proteins, Mice

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