| Texto completo | |
| Autor(es): |
Lima, Thiago Amorim de Souza
;
Ribeiro, Martina Raissa
;
de Brito, Malcon Carneiro
;
Kawamoto, Elisa Mitiko
Número total de Autores: 4
|
| Tipo de documento: | Artigo Científico |
| Fonte: | Neuroscience; v. 560, p. 10-pg., 2024-09-18. |
| Resumo | |
Type 1 diabetes mellitus (T1D) is associated with cognitive impairments in humans. A well-established animal model of T1D is induced through the administration of streptozotocin (STZ), a glucose analog that induces pancreatic (3-cell death, resulting in hyperglycemia and cognitive impairment linked to neuroinflammation and oxidative stress. Tumor necrosis factor (TNF)-a, a key inflammatory mediator, is elevated in the central nervous system (CNS) of diabetic animals. In this study, we utilized TNFR1 knockout mice to investigate the role of TNFR1 signaling in short-term T1D-related cognitive impairment. Our findings showed that diabetic animals did not develop cognitive damage within the first 2 weeks of T1D but exhibited reduced exploration in all behavioral tests. Our findings suggest that this reduction in exploration was attributable to motor impairment, as there was no reduction in motivated novelty-seeking behavior. Additionally, deletion of TNFR1 signaling attenuated gait speed impairment in diabetic mice, but did not affect other motor-related or exploratory behaviors. (AU) | |
| Processo FAPESP: | 16/22996-9 - Avaliação dos efeitos do exercício físico na cognição de animais com deleção da PTEN em neurônios |
| Beneficiário: | Elisa Mitiko Kawamoto Iwashe |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |