GLP-1 Analogues and neuroprotection: a systematic review

• Autor(a) principal: Castro, Júlia Vasconcellos
• Data de Publicação: 2023
• Outros Autores: Cruz, Thainá Baltazar Ferreira da, Fonseca, Isabela Oliveira, Tostes, Glauce Cordeio Ulhôa
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Brazilian Journal of Implantology and Health Sciences
• Texto Completo: https://bjihs.emnuvens.com.br/bjihs/article/view/600
• topic: GLP-1, Neuroproteção.; GLP-1, Neuroprotection.

Diabetes Mellitus 2 (DM2) is a chronic disease with growing incidence, resulting in increased morbidity and mortality due to associated complications, including neurodegeneration and structural changes, related to insulin resistance and hyperglycemia. Furthermore, insulinotropic hormones, such as GLP-1 receptor agonists, stimulate insulin stimulation and regulate blood glucose. Central activation of GLP-1R reduces appetite and also body weight, by increasing PKA and MAPK phosphorylation and promoting AMPK activity in the nucleus of the solitary tract. These impacts include increased supervision of neuron progenitor cells, prolonged hippocampal activation, improved learning, decreased oxidative stress, increased neurogenesis and synaptic plasticity, decreased neurotoxicity, and reduced the formation of beta-amyloid plaques. and neuroinflammation. Therefore, this study aimed to analyze, through a systematic literature review, the impacts of GLP-1 analogues on neuroprotection. A literature review was developed, qualitatively, trough data collected from electronic databases such as PudMed, Cochrane and Scielo, with searches by descriptors: “GLP-1”, “neuroprotection” and their variations according MeSH. The PRISMA scale was employed to systematize the study. Priority was given to controlled clinical trials, in humans, in English. The exclusion criteria were studies carried out in animals or that did not have a clear methodology or did not meet the inclusion criteria. Most articles demonstrate that GLP-1R stimulation is neurotrophic/neuroprotective, inducing cell differentiation and growth, and providing protection against apoptotic neuronal cell death caused by glutamate, and protects against oxidative stress and membrane lipid peroxidation. Therefore, GLP-1 RA provides cerebral vascular protection in patients with high risk for events, such as the diabetic population, and appears to be promising drugs for the treatment of dementia diseases, such as Alzheimer's disease in early stages. At last, more evaluated clinical trials with long-term follow-up are needed for a robust conclusion.