Background: Neurodegenerative diseases affect more than 65 million people worldwide and significantly reduce quality of life while contributing to a leading cause of global mortality. Disorders such as Alzheimer’s disease and Parkinson’s disease currently lack treatments that effectively slow disease progression. Modifiable risk factors of these diseases include diet, body mass index (BMI), and diabetes . Furthermore, Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), commonly used to treat type 2 diabetes and obesity, have recently shown potential neuroprotective effects, including reduced neuroinflammation and improved neuronal survival. Objective: This project hypothesizes that GLP-1 receptor agonists may reduce neurodegenerative disease progression through neuroprotective mechanisms independent of, or partially related to, glucose lowering. Methods: We conducted a systematized literature review by searching PubMed, Embase, Cochrane, and CINAHL. Inclusion criteria include studies that use semaglutide or other GLP-1 RAs and assess neuroprotective markers or neurological outcomes. Exclusion criteria include studies focused solely on weight loss or non-GLP-1 diabetes medications. Results: Preclinical studies have shown that GLP-1 agonists are a promising treatment for neurodegenerative diseases.
In Alzheimer’s disease mouse models treated with liraglutide (a GLP-1 agonist for mice), there was a decrease in β-Objective: This project hypothesizes that GLP-1 receptor agonists may reduce neurodegenerative disease progression through neuroprotective mechanisms independent of, or partially related to, glucose lowering. Methods: We conducted a systematized literature review by searching PubMed, Embase, Cochrane, and CINAHL. Inclusion criteria include studies that use semaglutide or other GLP-1 RAs and assess neuroprotective markers or neurological outcomes. Exclusion criteria include studies focused solely on weight loss or non-GLP-1 diabetes medications. Results: Preclinical studies have shown that GLP-1 agonists are a promising treatment for neurodegenerative diseases. In Alzheimer’s disease mouse models treated with liraglutide (a GLP-1 agonist for mice), there was a decrease in β-amyloid plaques and tau levels, which also led to a decrease in active microglia and an overall reduction in inflammation. In Parkinson’s disease mouse models treated with extendin-4 (a GLP-1 agonist), motor impairment decreased, and protection against loss of dopaminergic neurons was observed.
Conclusion: Overall, there is promising evidence supporting the use of GLP-1 agonists as a treatment for neurodegenerative diseases. The first clinical trial that was done showed that it was a safe drug to use for Alzheimer’s patients, but the study had too small a sample size to generate significant results. The next step is to conduct more clinical trials with larger experimental populations to further validate its effectiveness in preventing neurodegeneration in humans.
In Alzheimer’s disease mouse models treated with liraglutide (a GLP-1 agonist for mice), there was a decrease in β-Objective: This project hypothesizes that GLP-1 receptor agonists may reduce neurodegenerative disease progression through neuroprotective mechanisms independent of, or partially related to, glucose lowering. Methods: We conducted a systematized literature review by searching PubMed, Embase, Cochrane, and CINAHL. Inclusion criteria include studies that use semaglutide or other GLP-1 RAs and assess neuroprotective markers or neurological outcomes. Exclusion criteria include studies focused solely on weight loss or non-GLP-1 diabetes medications. Results: Preclinical studies have shown that GLP-1 agonists are a promising treatment for neurodegenerative diseases. In Alzheimer’s disease mouse models treated with liraglutide (a GLP-1 agonist for mice), there was a decrease in β-amyloid plaques and tau levels, which also led to a decrease in active microglia and an overall reduction in inflammation. In Parkinson’s disease mouse models treated with extendin-4 (a GLP-1 agonist), motor impairment decreased, and protection against loss of dopaminergic neurons was observed.
Conclusion: Overall, there is promising evidence supporting the use of GLP-1 agonists as a treatment for neurodegenerative diseases. The first clinical trial that was done showed that it was a safe drug to use for Alzheimer’s patients, but the study had too small a sample size to generate significant results. The next step is to conduct more clinical trials with larger experimental populations to further validate its effectiveness in preventing neurodegeneration in humans.