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Published on: May 28, 2017
Endomorphin-1 attenuates Aβ42 induced impairment of novel object and object location recognition tasks in mice
Rui-san Zhang1, Hong-jiao Xu1, Jin-hong Jiang1
1Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, PR China.
Abstract:
A growing body of evidence suggests that the agglomeration of amyloid-β (Aβ) may be a trigger for Alzheimer׳s disease (AD). Central infusion of Aβ42 can lead to memory impairment in mice. Inhibiting the aggregation of Aβ has been considered a therapeutic strategy for AD. Endomorphin-1 (EM-1), an endogenous agonist of μ-opioid receptors, has been shown to inhibit the aggregation of Aβ in vitro. In the present study, we investigated whether EM-1 could alleviate the memory-impairing effects of Aβ42 in mice using novel object recognition (NOR) and object location recognition (OLR) tasks. We showed that co-administration of EM-1 was able to ameliorate Aβ42-induced amnesia in the lateral ventricle and the hippocampus, and these effects could not be inhibited by naloxone, an antagonist of μ-opioid receptors. Infusion of EM-1 or naloxone separately into the lateral ventricle had no influence on memory in the tasks. These results suggested that EM-1 might be effective as a drug for AD preventative treatment by inhibiting Aβ aggregation directly as a molecular modifier.
Insights
Endomorphin-1 (EM-1) may offer a new therapeutic strategy for Alzheimer's disease (AD). This study shows EM-1 can reverse memory loss caused by amyloid-beta (Aβ) in mice, suggesting a direct molecular modification approach.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Amyloid-beta (Aβ) aggregation is implicated in Alzheimer's disease (AD) pathogenesis.
- Aβ42 infusion in mice induces memory deficits, making it a relevant model for AD research.
- Inhibiting Aβ aggregation is a key therapeutic strategy for AD.
Purpose of the Study:
- To investigate the efficacy of Endomorphin-1 (EM-1) in ameliorating Aβ42-induced memory impairment in mice.
- To explore the potential of EM-1 as a therapeutic agent for Alzheimer's disease.
Main Methods:
- Utilized novel object recognition (NOR) and object location recognition (OLR) tasks to assess memory function in mice.
- Administered Aβ42 and EM-1 centrally (lateral ventricle and hippocampus).
- Investigated the role of μ-opioid receptors by co-administering naloxone, a μ-opioid receptor antagonist.
Main Results:
- Co-administration of EM-1 significantly ameliorated Aβ42-induced amnesia in both the lateral ventricle and hippocampus.
- The memory-ameliorating effects of EM-1 were not blocked by naloxone, suggesting a mechanism independent of μ-opioid receptors.
- Separate administration of EM-1 or naloxone did not affect memory performance.
Conclusions:
- Endomorphin-1 demonstrates potential as a preventative treatment for Alzheimer's disease.
- EM-1 may exert its therapeutic effects by directly inhibiting amyloid-beta aggregation as a molecular modifier.
- The findings suggest a novel, non-opioid receptor-mediated therapeutic avenue for AD treatment.
