Department of Pharmaceutical Sciences, School of Pharmacy, College of Health Professions, North Dakota State University, Fargo, ND 58105, USA.
Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Int J Biol Macromol. 2022 May 31;208:901-911. doi: 10.1016/j.ijbiomac.2022.03.203. Epub 2022 Apr 2.
Brain-derived neurotrophic factor (BDNF) is actively produced and utilized in cortical circuits throughout life to sustain neuronal function and synaptic plasticity. In animal models of Alzheimer's Disease (AD), highly invasive BDNF gene therapy using viral vectors has successfully shown enhanced synaptic protein expression, proliferation of neurons and attenuation of amyloidogenic processes. However, to eliminate virus-related safety issues and invasive procedures, our present study has explored brain-targeted lipid-based nanoparticles that can deliver plasmid encoding BDNF to brain in a safe and efficient manner. Efficacy of these nanoparticles was tested in early (6-months) and advanced stage (9-months) transgenic APP/PS1 AD mice. Liposomes were surface-functionalized with brain targeting ligand, mannose, and cell-penetrating peptides (rabies virus-derived peptide or penetratin). These bifunctionalized nanoparticles enhanced BDNF expression by ~2 times and resulted in >40% (p < 0.05) reduction in toxic amyloid-beta peptides in 6- and 9-months old APP/PS1 mice brains compared to their age-matched untreated controls. Plaque load was reduced ~7 and ~3 times (p < 0.05), respectively, whereas synaptic proteins, synaptophysin and PSD-95, were found to be increased >90% (p < 0.05) in both age groups of transgenic mice treated with bifunctionalized nanoparticles. No untoward adverse effects were observed throughout treatment, suggesting a safe and effective strategy to rescue AD pathology.
脑源性神经营养因子(BDNF)在皮质回路中持续产生和利用,以维持神经元功能和突触可塑性。在阿尔茨海默病(AD)的动物模型中,使用病毒载体的高侵袭性 BDNF 基因治疗成功地显示了增强的突触蛋白表达、神经元增殖和淀粉样蛋白形成过程的衰减。然而,为了消除与病毒相关的安全问题和侵袭性程序,我们目前的研究探索了靶向大脑的基于脂质的纳米颗粒,这些纳米颗粒可以以安全有效的方式将编码 BDNF 的质粒递送到大脑。这些纳米颗粒的功效在早期(6 个月)和晚期(9 个月)转基因 APP/PS1 AD 小鼠中进行了测试。脂质体用脑靶向配体甘露糖和细胞穿透肽(狂犬病病毒衍生肽或 penetratin)进行表面功能化。与未经处理的年龄匹配对照相比,这些双功能化纳米颗粒使 BDNF 表达增加了约 2 倍,并导致 6 个月和 9 个月大的 APP/PS1 小鼠大脑中的毒性淀粉样β肽减少了超过 40%(p<0.05)。斑块负荷分别减少了约 7 倍和 3 倍(p<0.05),而突触蛋白突触小体和 PSD-95 在接受双功能化纳米颗粒治疗的两组转基因小鼠中均增加了超过 90%(p<0.05)。在整个治疗过程中没有观察到不良的不良反应,表明这是一种安全有效的策略,可以挽救 AD 病理。