ArticleCombinatorial chemistry & high throughput screening2025
Dulaglutide Alleviates Alzheimer's Disease by Regulating Microglial Polarization and Neurogenic Activity.
Article in Combinatorial chemistry & high throughput screening, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Pharmacoeconomic analysis (CER) of Dulaglutide and Liraglutide in the treatment of patients with type 2 diabetes.Frontiers in endocrinology · 2023Trial
- Xuebijing Alleviates Microglial Activation after Traumatic Brain Injury via Regulation of NF-κB Pathway: Network Pharmacology and Experimental Validation.Combinatorial chemistry & high throughput screening · 2026Article
- GLP-1R as a potential link between diabetes and Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- The Beneficial Effects of GLP-1 Receptor Agonists Other than Their Anti-Diabetic and Anti-Obesity Properties.Medicina (Kaunas, Lithuania) · 2024Review
- GLP-1/GIP Agonist as an Intriguing and Ultimate Remedy for Combating Alzheimer's Disease through its Supporting DPP4 Inhibitors: A Review.Current topics in medicinal chemistry · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing research has proved that microglial activation, polarization, and inflammatory response in the brain affect the pathology of Alzheimer's disease. Hence, employing reagents targeted to microglial functions to optimize the brain microenvironment may become a promising therapeutic method for Alzheimer's disease.
methodsThe phagocytosis and clearance of Aβ1-42 were detected using western blot and immunofluorescence assay. The cell viability was determined via 3-(4, 5-Dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) or cell counting kit-8 (CCK-8) assay. The load of proinflammation, in addition to anti-inflammation factors, was measured through an enzyme-linked immunosorbent (ELISA) assay. Flow cytometry was employed to estimate the apoptotic cells. The protein level related to microglial polarization and neuronal injury was detected via western blot. The length of the neuronal synapse was investigated using an immunofluorescence assay.
resultsDulaglutide significantly promoted microglia to phagocytose and removed the Aβ plague. Additionally, dulaglutide treatment inhibited the production of pro-inflammatory factors, including tumor necrosis factor (TNF)-α, interleukin -1β, and IL-6, whereas it increased the load of antiinflammatory molecules, such as IL-10 affected by Aβ1-42 exposure. Further investigation verified that Aβ1-42 down-regulated YM1/2 positive M2 microglial polarization phenotype but up-regulated cyclooxygenase-2 (Cox2) positive M1 microglia. However, treating with dulaglutide effectively counteracted these effects. Moreover, dulaglutide dramatically recovered primary cortical neuron cell viability and inhibited cell apoptosis influenced by Aβ1-42. Furthermore, the dulaglutide also reversed neuronal synapse injury after exposure to Aβ1-42.
conclusionAltogether, this investigation verified that dulaglutide improved Aβ-induced inflammation and neuronal injury by mediating the activation and polarization of microglia, thereby alleviating Alzheimer's disease efficiently.
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