ArticlePloS one2025
Semaglutide ameliorates diabetes-associated cognitive dysfunction in mouse model of type 2 diabetes.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Glucagon-Like Peptide-1 Signaling in Learning and Memory: Evidence, Mechanisms, and Therapeutic Implications.Biological psychiatry · 2026Review
- Semaglutide Attenuates Type 2 Diabetes-Induced Neurotoxicity by Modulating Neuroinflammation, Oxidative Stress, and Neuroapoptosis.Life (Basel, Switzerland) · 2026Article
- Semaglutide alters behaviour and nucleus accumbens oscillatory activity in healthy mice.Molecular brain · 2026Article
- Impact of Semaglutide on Hippocampal Injury in a Streptozotocin-Induced Model of Alzheimer's Disease.Biomedicines · 2026Article
- Sound pressure levels at 40 dB and 50 dB are more suitable for acoustic-cued water maze tests.BMC research notes · 2026Article
- Targeting neuroinflammation in neurodegenerative disorders: the emerging potential of semaglutide.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Metabolic inflammation at the adipose-brain axis.Frontiers in physiology · 2026Review
- Metabolic syndrome and perioperative neurocognitive disorders: epidemiology, mechanisms, and interventions.Frontiers in neuroscience · 2026Review
- Research Progress on Pathology, Molecular Mechanisms, and Intervention Strategies of Cognitive Dysfunction Associated with Type 2 Diabetes.International journal of general medicine · 2026Review
- Antidiabetic Agents as Antioxidant and Anti-Inflammatory Therapies in Neurological and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
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7 authors.
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Abstract
backgroundType 2 diabetes mellitus (T2DM) is associated with cognitive dysfunction, which significantly impacts the quality of life. Semaglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, has shown potential neuroprotective effects. This study investigates the efficacy of semaglutide in ameliorating cognitive dysfunction in a mouse model of T2DM.
methodsMale C57BL/6J mice were fed a high-fat diet for four weeks and received a single intraperitoneal injection of streptozotocin (150 mg/kg) to induce T2DM. All mice were divided into four groups: control, diabetes control (T2DM), semaglutide treatment (semaglutide, 0.1 mg/kg) and dapagliflozin treatment (dapagliflozin 1 mg/kg). Cognitive function was assessed using the Morris water maze (MWM) test. Histomorphological analysis of hippocampal tissues was performed using H&E and Nissl staining. Immunofluorescence was used to assess LRP1 expression and apoptosis. Biochemical analyses measured oxidative stress markers (SOD, MDA) and inflammatory cytokines (IL-1β, IL-6, TNF-α, CRP).
resultsSemaglutide treatment significantly reduced blood glucose levels in diabetic mice. In the MWM test, semaglutide-treated mice showed reduced escape latencies, indicating improved spatial learning and memory. Histomorphological analysis revealed preserved neuronal structure in the hippocampus with reduced neuronal damage and apoptosis in the semaglutide-treated group. Immunofluorescence showed increased LRP1 expression and decreased apoptosis. Biochemical analyses indicated that semaglutide reduced oxidative stress and inflammatory markers, further supporting its neuroprotective effects.
conclusionsSemaglutide effectively ameliorates cognitive dysfunction in T2DM mice, likely through mechanisms involving the reduction of oxidative stress, inflammation, and neuronal apoptosis. These findings suggest that semaglutide has potential as a therapeutic agent for managing diabetes-associated cognitive decline. Further research, including long-term studies and clinical trials, is necessary to validate these findings and explore the broader applicability of semaglutide in treating cognitive impairments in diabetic patients.
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