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Evaluation of the impact of Semaglutide on cognitive health and the progression of neurodegenerative diseases
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Keywords

Semaglutide
Cognition
Neurodegeneration

How to Cite

Evaluation of the impact of Semaglutide on cognitive health and the progression of neurodegenerative diseases. (2025). Revista Eletrônica Acervo Científico, 25, e20650. https://doi.org/10.25248/reac.e20650.2025

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Abstract

Objective: To evaluate the clinical impact of semaglutide on cognition and the progression of neurodegenerative diseases. Literature review: Semaglutide, a GLP-1 receptor agonist widely used in the treatment of type 2 diabetes and obesity, has shown effects beyond glycemic control, including neuroprotective benefits. Through a review of recent scientific literature, evidence was gathered highlighting semaglutide’s ability to cross the blood-brain barrier, modulate inflammatory processes in the central nervous system, preserve mitochondrial integrity, and promote neuronal homeostasis. These mechanisms may contribute to the reduction of cognitive decline and the progression of diseases such as Alzheimer’s and Parkinson’s. Final considerations: Based on the findings, it is concluded that semaglutide may represent an innovative therapeutic intervention in the field of neuroscience, especially in the management of neurodegenerative diseases. However, it is essential that more robust and specific clinical studies be conducted to confirm these effects, establish neurological treatment protocols, and ensure long-term safety in patients with cognitive impairment.

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References

ABADIN X, et al. Neuroinflammation in age-related neurodegenerative diseases: Role of mitochondrial oxidative stress. Antioxidants (Basel, Switzerland), 2024; 13(12): 1440.

ANDERBERG RH, et al. Glucagon-Like Peptide 1 and Its Analogs Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight. Diabetes, 2017; 66(4): 1062–1073.

ARNOLD SE, et al. Brain insulin resistance in type 2 diabetes and Alzheimer disease: concepts and conundrums. Nat Rev Neurol, 2018; 14(3): 168–181.

ASTER VKAKAJC. Robbins & Cotran Patologia: Bases Patológicas das Doenças. 10. ed. Rio de Janeiro: Grupo GEN, 2013; 3–1353.

BADULESCU S, et al. Glucagon-like peptide 1 agonist and effects on reward behaviour: A systematic review. Physiol Behav, 2024; 283: 114622.

CAO L, et al. Glucagon-like peptide-1 receptor agonist treatment improves insulin signaling in the brains of Alzheimer's disease models. Journal of Alzheimer's Disease, 2018; 66(3): 765–778.

CHOPRA G, et al. Proteinopathies: Deciphering physiology and mechanisms to develop effective therapies for neurodegenerative diseases. Molecular Neurobiology, 2022; 59(12): 7513–7540.

DOU X, et al. Effect and mechanism of GLP-1 on cognitive function in diabetes mellitus. Frontiers in neuroscience, 2025; 19: 1537898.

DURAN M, et al. Integration of Glucagon-Like Peptide 1 Receptor Actions Through the Central Amygdala. Endocrinology, 2025; 166(3): 19.

HENI M, et al. Impaired insulin action in the human brain: causes and metabolic consequences. Nat Rev Endocrinol, 2015; 11: 701–711.

HÖLSCHER C. Brain insulin resistance: a treatment target for Alzheimer's disease. Trends in Endocrinology and Metabolism, 2020; 31(4): 181–193.

HOULDSWORTH A. Role of oxidative stress in neurodegenerative disorders: a review of reactive oxygen species and prevention by antioxidants. Brain Communications, 2024; 6(1): 356.

HUANG Z, et al. Glucose-sensing glucagon-like peptide-1 receptor neurons in the dorsomedial hypothalamus regulate glucose metabolism. Sci Adv, 2022; 8(23): 5345.

MICHAELIS XWAEK. Selective neuronal vulnerability to oxidative stress in the brain. Frontier in, University of Kansas, 2010; 2(12): 1–13.

NOWELL J, et al. Dual GLP-1/GIP receptor agonists enhance neuroprotection and cognitive function in models of Alzheimer's disease. Neuropharmacology, 2023; 225: 109388.

NOWELL J, et al. Incretin and insulin signaling as novel therapeutic targets for Alzheimer’s and Parkinson’s disease. Mol Psychiatry, 2023; 28: 217–229.

REICH D, et al. Anti-inflammatory effects of semaglutide in patients with type 2 diabetes: a randomized controlled trial. Diabetes Therapy, 2023; 14(2): 399–412.

SILVA ACC, et al. A resistência à insulina no desenvolvimento da doença de Alzheimer: uma revisão narrativa. Revista Eletrônica Acervo Saúde, 2022; 15(1): 9300.

TANG BL. Glucose, glycolysis, and neurodegenerative diseases. Journal of Cellular Physiology, 2020; 235(11): 7653–7662.

TIMPER K, et al. GLP-1 Receptor Signaling in Astrocytes Regulates Fatty Acid Oxidation, Mitochondrial Integrity, and Function. Cell Metabolism, 2020; 31(6): 1189–1205.

WILSON DM, et al. Hallmarks of neurodegenerative diseases. Cell, 2023; 186(4): 693–714.

ZHANG L, et al. GLP-1 receptor agonist exendin-4 reduces oxidative stress and improves cognitive impairment in Alzheimer's disease model mice. Neuroscience Letters, 2018; 705: 41–48.