Khan Tapabrata, Thamaraikani Tamilanban, Vellapandian Chitra
Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology (SRMIST), Chennai, IND.
Pharmacy/Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology (SRMIST), Chengalpattu, IND.
Cureus. 2024 Aug 17;16(8):e67093. doi: 10.7759/cureus.67093. eCollection 2024 Aug.
A huge number of new cases - around a few million of traumatic brain injury (TBI) - are recorded globally each year, making it a major public health risk. A significant portion of all accident-related deaths are attributable to TBI, a notable mortality rate. There are TBI deaths in every age range. Long-term neurobehavioral impacts, such as altered emotions and personalities, cognitive and mental deficits, and so on, are experienced by the majority of survivors. Our main objective is to understand the possible mechanism of the NLRP3 inflammasome in retinal neurons and enhance precision regarding reducing the burden of retinal neurodegeneration in TBI-induced AD. Both primary and secondary insults initiate the intricate pathophysiology of traumatic brain injury. Primary injuries are caused by mechanical force and occur right after the collision. Long-lasting and delayed secondary injuries follow. Studies demonstrating the continuous nature of research on the relationship between retinal neurons and TBI-induced Alzheimer's disease (AD) include neurodegeneration, retinal changes, and inflammatory response biomarkers. TBI can cause changes that resemble those seen in AD. This includes the accumulation of tau tangles and amyloid-beta plaques, which are also observed in the retina and imply a potential relationship between AD, traumatic brain injury, and retinal health. The linkage between TBI and AD, the effect of the innate immune system in post-TBI AD, the function of immunological moderators, the activation and assembly of inflammasomes in TBI, the pathophysiology of TBI, and the connection between TBI and inflammasome activity were the main topics of discussion in the following discussions. Of particular interest was the potential mechanism by which the NLRP3 inflammasome, in conjunction with SREBP2 and SCAP inflammasome, in retinal neurons in TBI-induced AD. The thinning of RNFL, poor lipid metabolism, and new developments such as drug delivery technologies, lipid metabolism modulation in retinal neurons, and drug-targeting lipid pathways and their mechanisms are then covered in this article.
全球每年记录有大量新的创伤性脑损伤（TBI）病例——约数百万例，使其成为一项重大的公共卫生风险。所有与事故相关的死亡中，很大一部分可归因于TBI，死亡率显著。各个年龄段都有TBI死亡病例。大多数幸存者会经历长期的神经行为影响，如情绪和性格改变、认知和精神缺陷等。我们的主要目标是了解NLRP3炎性小体在视网膜神经元中的可能机制，并提高减轻TBI诱导的AD中视网膜神经变性负担的精准度。原发性和继发性损伤都会引发创伤性脑损伤复杂的病理生理学过程。原发性损伤由机械力引起，在碰撞后立即发生。随后是持久且延迟的继发性损伤。证明视网膜神经元与TBI诱导的阿尔茨海默病（AD）之间关系的持续性研究包括神经变性、视网膜变化和炎症反应生物标志物。TBI可导致类似于AD中所见的变化。这包括tau缠结和β淀粉样蛋白斑块的积累，在视网膜中也观察到这些现象，这意味着AD、创伤性脑损伤和视网膜健康之间存在潜在关系。TBI与AD之间的联系、先天免疫系统在TBI后AD中的作用、免疫调节剂的功能、TBI中炎性小体的激活和组装、TBI的病理生理学以及TBI与炎性小体活性之间的联系是后续讨论的主要话题。特别令人感兴趣的是NLRP3炎性小体与SREBP2和SCAP炎性小体在TBI诱导的AD的视网膜神经元中的潜在机制。本文随后涵盖了视网膜神经纤维层变薄、脂质代谢不良以及药物递送技术、视网膜神经元脂质代谢调节和药物靶向脂质途径及其机制等新进展。
