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GLP-1RAs such as semaglutide can effectively slow down the progression of Parkinson's disease. "New England Journal of Medicine" published an article

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Update time : 2024-04-09 15:29:14
On April 3, 2024, the New England Journal of Medicine (NEJM) published the results of a remarkable clinical trial: patients with early-stage Parkinson's disease who received lixisenatide for 12 months had better exercise than placebo. Obstacle progression is significantly slowed down! The NEJM review emphasized that if this effect can be enhanced as treatment continues, GLP-1 therapy is expected to become an emerging strategy that changes the treatment landscape of Parkinson's disease.


clinical trial design
 
The LIXIPARK trial announced this time is a phase 2, multi-center, double-blind, parallel, randomized, placebo-controlled trial initiated by French researchers. It aims to evaluate the efficacy of GLP-1RA lixisenatide compared with placebo. Impact on the progression of movement disorders in patients with PD.
 
The LIXIPARK trial announced this time is a multi-center, double-blind, randomized, placebo-controlled trial designed to evaluate the effect of GLP-1RA lixisenatide on the progression of dyskinesia in patients with PD. Researchers recruited 156 patients with mild to moderate PD from the French Parkinson's Disease and Movement Disorders Clinical Research Network and randomly assigned them 1:1 to receive lixisenatide or placebo for 12 months. The primary endpoint of the trial is to assess patients' level of dyskinesia, as measured by change from baseline in Part III of the Parkinson's Disease Rating Scale (MDS-UPDRS).
 
The results showed that at 12 months, the score change in the lixisenatide group was -0.04 (improvement) and the placebo group score change was 3.04 (worsening) , and the difference between the two was statistically significant. At 14 months, after a 2-month washout period, the MDS-UPDRS motor score in the non-administration state was 17.7 in the lixisenatide group and 20.6 in the placebo group. 46% of participants in the lixisenatide group experienced nausea and 13% experienced vomiting.


Research result
Previous studies have shown that neuroinflammation is an important factor in the pathogenesis of PD. Based on the detection of inflammatory biomarkers in the blood and cerebrospinal fluid of PD patients, the correlation between neuroinflammation and the occurrence and progression of PD is further confirmed. Although GLP-1 receptor activation triggers a variety of physiological effects in patients, this class of drugs is known to be effective in reducing brain inflammation in patients.
 
In a 12-month phase 2 trial, the subcutaneous GLP-1RA lixisenatide slowed the progression of dyskinesia in patients with early-stage PD compared with placebo. Although the magnitude of the change in this finding is small, its importance lies in the potential effects it portends. If the benefits of GLP-1RA drugs like lixisenatide in PD patients can be cumulative, for example, a 3-point reduction per year over 5 to 10 years or more, this could be a truly transformative treatment. Follow-up larger-scale and long-term trials are needed to determine the effectiveness and safety of this drug in treating PD, and whether it has a significant effect in changing disease progression.


▍The dual power of GLP-1 such as semaglutide: the hope of suppressing inflammation and treating Parkinson’s and Alzheimer’s disease

January 26, 2024 A landmark study finds that a popular weight-loss drug not only effectively reduces weight but also plays a role in suppressing inflammation in organs, particularly in the brain. The discovery brings new hope for treating Parkinson's disease and Alzheimer's disease.
         

GLP-1 receptor agonists, including semaglutide and tilpotide , have been shown to reduce inflammatory responses in the liver, kidneys and heart. Even more surprising is that the drugs appear to reduce inflammation in the brain, which could provide new ideas for using compounds to treat Parkinson's and Alzheimer's diseases.A recent review paper lists multiple clinical trials that are exploring these drugs as treatments for both diseases.

 

"The next generation of drugs may be more targeted at reducing the new inflammatory pathways that we have identified," said Dr. Daniel Drucker, an endocrinologist at the University of Toronto. "Maybe they will be more effective "
 

The anti-inflammatory ability of GLP-1RA mainly originates from the brain

Recently, a study led by Daniel Drucker of the University of Toronto, Canada, winner of the 2023 Wolf Prize in Medicine, found that the anti-inflammatory ability of GLP-1RA mainly originates from the brain.

 

Mechanistically, GLP-1RA penetrates the blood-brain barrier and activates the glucagon-like peptide-1 receptor (GLP-1R) in the central nervous system of the brain. GLP-1R further indirectly inhibits Toll-like receptor (TLR) agonist-mediated pro-inflammatory cytokines through α1-adrenoceptor, δ-opioid receptor, and κ-opioid receptor signaling, i.e., plasma tumors Production of necrosis factor alpha (TNF-α).

 

This discovery not only confirms for the first time the existence of a GLP-1-brain-immune axis that is initiated by GLP-1RA to achieve immune regulation through the central nervous system, but also expands the emerging concept of brain-immune network in recent years.

In the study, the experimenters induced systemic inflammation by injecting mice with bacterial cell wall components or bacterial sludge to induce sepsis - a widespread inflammation of the body that can lead to organ damage.

 

Notably, GLP-1 RA reduces inflammation, but only if its receptors in the brain are not blocked. When these brain receptors were pharmacologically inhibited or genetically removed in mice, the drugs lost their ability to reduce inflammation.

 

The results of this study demonstrate for the first time that the "GLP-1-brain-immune axis" can regulate systemic inflammatory status independent of weight loss, even in peripheral organs without GLP-1 receptors.
             

"What's strange is that in all the other organs where GLP-1 agonists seem to work, you don't find many GLP-1 receptors, " says Dr. Drucker. Dr. Drucker suggests that this may be related to the brain for two reasons: One is that there are a large number of GLP-1 receptors in the brain, and the other is that the brain and immune system are connected to all organs of the body.

 

The new study is far from complete. The authors are now trying to identify the brain cells that interact with GLP-1. They are also studying multiple mouse models of inflammation (including heart disease, atherosclerosis, liver and kidney inflammation) to determine whether the effectiveness of GLP-1 agonists in each model is indeed mediated through the brain. .

 

Understanding how GLP-1 agonists suppress inflammation may open new avenues for reducing complications associated with type 2 diabetes and obesity, Dr. Drucker said.

*This article is for reference only by medical and health professionals
 


 

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