A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease

Parkinson’s disease (PD) is a complex syndrome with many elements, such as chronic inflammation, oxidative stress, mitochondrial dysfunction, loss of dopaminergic neurons, build-up of alpha-synuclein (α-syn) in cells, and energy depletion in neurons, that drive the disease. We and others have shown...

Full description

Saved in:
Bibliographic Details
Main Authors: Zijuan Zhang, Ming Shi, Zhengmin Li, Yuan Ling, Luke Zhai, Ye Yuan, He Ma, Li Hao, Zhonghua Li, Zhenqiang Zhang, Christian Hölscher
Format: Article
Language:English
Published: Wiley 2023-01-01
Series:Parkinson's Disease
Online Access:http://dx.doi.org/10.1155/2023/7427136
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849701499087618048
author Zijuan Zhang
Ming Shi
Zhengmin Li
Yuan Ling
Luke Zhai
Ye Yuan
He Ma
Li Hao
Zhonghua Li
Zhenqiang Zhang
Christian Hölscher
author_facet Zijuan Zhang
Ming Shi
Zhengmin Li
Yuan Ling
Luke Zhai
Ye Yuan
He Ma
Li Hao
Zhonghua Li
Zhenqiang Zhang
Christian Hölscher
author_sort Zijuan Zhang
collection DOAJ
description Parkinson’s disease (PD) is a complex syndrome with many elements, such as chronic inflammation, oxidative stress, mitochondrial dysfunction, loss of dopaminergic neurons, build-up of alpha-synuclein (α-syn) in cells, and energy depletion in neurons, that drive the disease. We and others have shown that treatment with mimetics of the growth factor glucagon-like peptide 1 (GLP-1) can normalize energy utilization, neuronal survival, and dopamine levels and reduce inflammation. Liraglutide is a GLP-1 analogue that recently showed protective effects in phase 2 clinical trials in PD patients and in Alzheimer disease patients. We have developed a novel dual GLP-1/GIP receptor agonist that can cross the blood-brain barrier and showed good protective effects in animal models of PD. Here, we test liraglutide against the dual GLP-1/GIP agonist DA5-CH (KP405) in the A53T tg mouse model of PD which expresses a human-mutated gene of α-synuclein. Drug treatment reduced impairments in three different motor tests, reduced levels of α-syn in the substantia nigra, reduced the inflammation response and proinflammatory cytokine levels in the substantia nigra and striatum, and normalized biomarker levels of autophagy and mitochondrial activities in A53T mice. DA5-CH was superior in almost all parameters measured and therefore may be a better drug treatment for PD than liraglutide.
format Article
id doaj-art-20af0c45b2a5462f92f8fe168ae8f85d
institution DOAJ
issn 2042-0080
language English
publishDate 2023-01-01
publisher Wiley
record_format Article
series Parkinson's Disease
spelling doaj-art-20af0c45b2a5462f92f8fe168ae8f85d2025-08-20T03:17:55ZengWileyParkinson's Disease2042-00802023-01-01202310.1155/2023/7427136A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s DiseaseZijuan Zhang0Ming Shi1Zhengmin Li2Yuan Ling3Luke Zhai4Ye Yuan5He Ma6Li Hao7Zhonghua Li8Zhenqiang Zhang9Christian Hölscher10School of Medical SciencesSchool of Medical SciencesSchool of Medical SciencesAcademy of Chinese Medical SciencesAcademy of Chinese Medical SciencesAcademy of Chinese Medical SciencesAcademy of Chinese Medical SciencesSchool of Medical SciencesAcademy of Chinese Medical SciencesAcademy of Chinese Medical SciencesAcademy of Chinese Medical SciencesParkinson’s disease (PD) is a complex syndrome with many elements, such as chronic inflammation, oxidative stress, mitochondrial dysfunction, loss of dopaminergic neurons, build-up of alpha-synuclein (α-syn) in cells, and energy depletion in neurons, that drive the disease. We and others have shown that treatment with mimetics of the growth factor glucagon-like peptide 1 (GLP-1) can normalize energy utilization, neuronal survival, and dopamine levels and reduce inflammation. Liraglutide is a GLP-1 analogue that recently showed protective effects in phase 2 clinical trials in PD patients and in Alzheimer disease patients. We have developed a novel dual GLP-1/GIP receptor agonist that can cross the blood-brain barrier and showed good protective effects in animal models of PD. Here, we test liraglutide against the dual GLP-1/GIP agonist DA5-CH (KP405) in the A53T tg mouse model of PD which expresses a human-mutated gene of α-synuclein. Drug treatment reduced impairments in three different motor tests, reduced levels of α-syn in the substantia nigra, reduced the inflammation response and proinflammatory cytokine levels in the substantia nigra and striatum, and normalized biomarker levels of autophagy and mitochondrial activities in A53T mice. DA5-CH was superior in almost all parameters measured and therefore may be a better drug treatment for PD than liraglutide.http://dx.doi.org/10.1155/2023/7427136
spellingShingle Zijuan Zhang
Ming Shi
Zhengmin Li
Yuan Ling
Luke Zhai
Ye Yuan
He Ma
Li Hao
Zhonghua Li
Zhenqiang Zhang
Christian Hölscher
A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
Parkinson's Disease
title A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
title_full A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
title_fullStr A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
title_full_unstemmed A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
title_short A Dual GLP-1/GIP Receptor Agonist Is More Effective than Liraglutide in the A53T Mouse Model of Parkinson’s Disease
title_sort dual glp 1 gip receptor agonist is more effective than liraglutide in the a53t mouse model of parkinson s disease
url http://dx.doi.org/10.1155/2023/7427136
work_keys_str_mv AT zijuanzhang adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT mingshi adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhengminli adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT yuanling adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT lukezhai adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT yeyuan adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT hema adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT lihao adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhonghuali adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhenqiangzhang adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT christianholscher adualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zijuanzhang dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT mingshi dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhengminli dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT yuanling dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT lukezhai dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT yeyuan dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT hema dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT lihao dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhonghuali dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT zhenqiangzhang dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease
AT christianholscher dualglp1gipreceptoragonistismoreeffectivethanliraglutideinthea53tmousemodelofparkinsonsdisease