Skip to main content
U.S. flag

An official website of the United States government

A GLP-1/GIP dual receptor agonist DA4-JC effectively attenuates cognitive impairment and pathology in the APP/PS1/Tau model of Alzheimer’s disease

Bibliographic

Year of Publication:
2021
Contact PI Name:
Christian Holscher
Contact PI Affiliation:
Neuroscience Research Group, Henan University of Chinese Medicine, Zhengzhou, China
Co-Authors:
Hong-Yan Cai, Dan Yanga, Jing Qiao, Jun-Ting Yang, Zhao-Jun Wang, Mei-Na Wu, Jin-Shun Q
Primary Reference (PubMED ID):
Funding Source:
National Natural Science Foundation of China
Ministry of Education of China
Fund for Shanxi 1331 Project Key Subjects Construction
Key Laboratory of Cellular Physiology of Shanxi Medical University
Shanxi Scholarship Council of China
Study Goal and Principal Findings:

Background: Alzheimer's disease (AD) is a degenerative disorder, accompanied by progressive cognitive decline, for which there is no cure. Recently, the close correlation between AD and type 2 diabetes mellitus (T2DM) has been noted, and a promising anti-AD strategy is the use of anti-T2DM drugs.

Objective: To investigate if the novel glucagon-like peptide-1 (GLP-1)/glucose-dependent insulinotropic polypeptide (GIP) receptor agonist DA4-JC shows protective effects in the triple APP/PS1/tau mouse model of AD.

Methods: A battery of behavioral tests were followed by in vivo recording of long-term potentiation (LTP) in the hippocampus, quantified synapses using the Golgi method, and biochemical analysis of biomarkers.

Results: DA4-JC improved cognitive impairment in a range of tests and relieved pathological features of APP/PS1/tau mice, enhanced LTP in the hippocampus, increased numbers of synapses and dendritic spines, upregulating levels of post-synaptic density protein 95 (PSD95) and synaptophysin (SYP), normalized volume and numbers of mitochondria and improving the phosphatase and tensin homologue induced putative kinase 1 (PINK1) - Parkin mitophagy signaling pathway, while downregulating amyloid, p-tau, and autophagy marker P62 levels.

Conclusion: DA4-JC is a promising drug for the treatment of AD.

Bibliographic Notes:
Hong-Yan Cai (Department of Microbiology and Immunology, Shanxi Medical University, Taiyuan, China) and Christian Holscher (Neuroscience Research Group, Henan University of Chinese Medicine, Zhengzhou, China) are corresponding authors on this paper.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Biologic - Peptide
Therapeutic Agent:
DA4-JC
Therapeutic Target:
Glucagon-Like Peptide 1 Receptor (GLP-1R)
Therapeutic Target:
Glucose-Dependent Insulinotropic Polypeptide (GIP) Receptor

Animal Model

Model Information:
Species:
Mouse
Model Type:
APPxPS1xTau
Strain/Genetic Background:
Not Reported
Species:
Mouse
Model Type:
Non-transgenic
Strain/Genetic Background:
C57BL/6J

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
Contextual Fear Conditioning
Exploratory Activity
Morris Water Maze
Novel Object Recognition Test (NORT)
Open Field Test
Spontaneous Alternation
Y Maze
Motor Function
Locomotor Activity
Path Length
Swimming Speed
Histopathology
beta Amyloid Deposits
phospho-Tau
Synaptic Loss
Biochemical
p62/Sequestosome 1 (SQSTM1)
Parkin
Postsynaptic Density Protein 95 (PSD95)
PTEN Induced Kinase 1 (PINK1)
Synaptophysin
Immunochemistry
Brain-beta Amyloid Deposits
phospho-Tau
Microscopy
Dendritic Spine Number
Dendritic Spine Density
Electron Microscopy
Mitochondria Count
Mitochondria Morphology
Synaptic Density
Spectroscopy
Matrix-Assisted Laser Desorption/Ionization-Time of Flight (MALDI-TOF) Mass Spectrometry
Electrophysiology
field Excitatory Postsynaptic Potential (fEPSP)
Input/Output (I/O) Curve
Long Term Potentiation (LTP)
Paired-Pulse Facilitation (PPF)
Toxicology
Body Weight