International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden.
Department of Neurology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, China.
Adv Neurobiol. 2023;32:3-53. doi: 10.1007/978-3-031-32997-5_1.
Sleep deprivation induces amyloid beta peptide and phosphorylated tau deposits in the brain and cerebrospinal fluid together with altered serotonin metabolism. Thus, it is likely that sleep deprivation is one of the predisposing factors in precipitating Alzheimer's disease (AD) brain pathology. Our previous studies indicate significant brain pathology following sleep deprivation or AD. Keeping these views in consideration in this review, nanodelivery of monoclonal antibodies to amyloid beta peptide (AβP), phosphorylated tau (p-tau), and tumor necrosis factor alpha (TNF-α) in sleep deprivation-induced AD is discussed based on our own investigations. Our results suggest that nanowired delivery of monoclonal antibodies to AβP with p-tau and TNF-α induces superior neuroprotection in AD caused by sleep deprivation, not reported earlier.
睡眠剥夺会导致大脑和脑脊液中淀粉样β肽和磷酸化 tau 沉积，以及 5-羟色胺代谢改变。因此，睡眠剥夺可能是促使阿尔茨海默病（AD）脑病理学发生的一个诱发因素。我们之前的研究表明，睡眠剥夺或 AD 后会出现明显的脑病理学。基于我们自己的研究，在本次综述中，我们在这些观点的基础上，探讨了睡眠剥夺诱导的 AD 中单克隆抗体针对淀粉样β肽（AβP）、磷酸化 tau（p-tau）和肿瘤坏死因子α（TNF-α）的纳米递药。我们的结果表明，纳米线递药将 AβP 与 p-tau 和 TNF-α 一起递送至 AD 中，可诱导睡眠剥夺引起的 AD 产生更好的神经保护作用，这是之前未曾报道过的。
