Ceftriaxone alleviates mitochondrial damage through the inhibition of extrasynaptic NMDA receptor-mediated changes in intracellular calcium levels to improve cognitive deficits in APP/PS1 mice.
第一作者:
Li-Rong,Liu
第一单位:
Department of Pathophysiology, Neuroscience Research Center, Hebei Key Laboratory of Critical Disease Mechanism and Intervention, Hebei Medical University, 361 Zhongshan East Road, Shijiazhuang, 050017, P. R. China.
作者:
医学主题词
动物(Animals);头孢曲松(Ceftriaxone);线粒体(Mitochondria);小鼠(Mice);钙(Calcium);受体, N-甲基-D-天冬氨酸(Receptors, N-Methyl-D-Aspartate);小鼠, 转基因(Mice, Transgenic);小鼠, 近交C57BL(Mice, Inbred C57BL);早老素1(Presenilin-1);男(雄)性(Male);淀粉样β蛋白前体(Amyloid beta-Protein Precursor);疾病模型, 动物(Disease Models, Animal);阿尔茨海默病(Alzheimer Disease);海马(Hippocampus);兴奋性氨基酸转运子2(Excitatory Amino Acid Transporter 2)
DOI
10.1186/s13195-025-01900-w
PMID
41327376
发布时间
2026-05-14
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