Fonte: Brain Research. Unidade: ICB
Assuntos: FISIOLOGIA, FARMACOLOGIA, CAMUNDONGOS, MODELOS ANIMAIS DE DOENÇAS, DOENÇA DE PARKINSON, INFLAMAÇÃO, CITOCINAS, NECROSE
ABNT
CABRAL, Laís M. et al. TNFR1-mediated neuroinflammation is necessary for respiratory deficits observed in 6-hydroxydopamine mouse model of Parkinsońs Disease. Brain Research, v. 1822, 2024Tradução . . Disponível em: https://doi.org/10.1016/j.brainres.2023.148586. Acesso em: 31 out. 2024.APA
Cabral, L. M., Oliveira, L. M., Miranda, N. C., Kawamoto, E. M., Costa, S. K. P., Moreira, T. S., & Takakura, A. C. (2024). TNFR1-mediated neuroinflammation is necessary for respiratory deficits observed in 6-hydroxydopamine mouse model of Parkinsońs Disease. Brain Research, 1822. doi:10.1016/j.brainres.2023.148586NLM
Cabral LM, Oliveira LM, Miranda NC, Kawamoto EM, Costa SKP, Moreira TS, Takakura AC. TNFR1-mediated neuroinflammation is necessary for respiratory deficits observed in 6-hydroxydopamine mouse model of Parkinsońs Disease [Internet]. Brain Research. 2024 ; 1822[citado 2024 out. 31 ] Available from: https://doi.org/10.1016/j.brainres.2023.148586Vancouver
Cabral LM, Oliveira LM, Miranda NC, Kawamoto EM, Costa SKP, Moreira TS, Takakura AC. TNFR1-mediated neuroinflammation is necessary for respiratory deficits observed in 6-hydroxydopamine mouse model of Parkinsońs Disease [Internet]. Brain Research. 2024 ; 1822[citado 2024 out. 31 ] Available from: https://doi.org/10.1016/j.brainres.2023.148586