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Royal jelly alleviates cognitive deficits and β-amyloid accumulation in APP/PS1 mouse model via activation of the cAMP/PKA/CREB/BDNF pathway and inhibition of neuronal apoptosis

Bibliographic

Year of Publication:
2019
Contact PI Name:
Fuliang Hu
Contact PI Affiliation:
College of Animal Sciences, Zhejiang University, Hangzhou, China
Co-Authors:
Mengmeng You, Yongming Pan, Yichen Liu, Yifan Chen, Yuqi Wu, Juanjuan Si, Kai Wang
Primary Reference (PubMED ID):
Funding Source:
Modern Agro-industry Technology Research System from the Ministry of Agriculture of China
National Natural Science Foundation of China
Study Goal and Principal Findings:

Alzheimer’s disease (AD) is characterized clinically by progressive cognitive decline and pathologically by the accumulation of amyloid-β (Aβ) in the brain. Royal jelly (RJ), a secretion of honeybee hypopharyngeal and mandibular glands, has previously been shown to have anti-aging and neuromodulatory activities. In this study, we discovered that 3 months of RJ treatment substantially ameliorated behavioral deficits of APP/PS1 mice in the Morris Water Maze (MWM) test and step-down passive avoidance test. Our data also showed that RJ significantly diminished amyloid plaque pathology in APP/PS1 mice. Furthermore, RJ alleviated c-Jun N-terminal kinase (JNK) phosphorylation-induced neuronal apoptosis by suppressing oxidative stress. Importantly, hippocampal cyclic adenosine monophosphate (cAMP), p-PKA, p-CREB and BDNF levels were significantly increased in the APP/PS1 mice after RJ treatment, indicating that the cAMP/PKA/CREB/BDNF pathway might be related to the ameliorative effect of RJ on cognitive decline. Collectively, these results provide a scientific basis for using RJ as a functional food for targeting AD pathology.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Interventions & Supplements
Therapeutic Agent:
Royal Jelly
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Species:
Mouse
Model Type:
APPxPS1
Strain/Genetic Background:
C57BL/6

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest

Outcomes

Outcome Measured
Outcome Parameters
Behavioral
Morris Water Maze
Step-Down Passive Avoidance Test
Histopathology
Fibrillar Plaques
Fibrillar beta Amyloid Deposits
beta Amyloid Deposits
beta Amyloid Load
Biochemical
Malondialdehyde (MDA)
Cyclic Adenosine Monophosphate (cAMP)
cAMP Response Element-Binding Protein (CREB)
phospho-cAMP Response Element-Binding Protein (phospho-CREB)
Brain-Detergent Soluble beta Amyloid Peptide 40
Brain-Detergent Soluble beta Amyloid Peptide 42
beta-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1)
Low Density Lipoprotein Receptor-Related Protein 1 (LRP1)
Neprilysin
Insulin Degrading Enzyme (IDE)
Protein Kinase A (PKA)
phospho-Protein Kinase A (phospho-PKA)
Bcl-2
Bax
Cleaved Caspase 3
Cleaved Caspase 9
Brain-Derived Neurotrophic Factor (BDNF)
phospho-c-Jun N-terminal Kinase (phospho-JNK)
Brain-beta Amyloid Peptide-Total
Immunochemistry
Insulin Degrading Enzyme (IDE)
beta-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1)
Toxicology
Body Weight