Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite D, New Orleans, LA 70112, USA.
Mol Neurobiol. 2012 Aug;46(1):221-6. doi: 10.1007/s12035-012-8322-5. Epub 2012 Sep 7.
Neurodegenerative diseases encompass complex cell signaling disturbances that initially damage neuronal circuits and synapses. Due to multiple protective mechanisms enacted to counteract the onset of neurodegenerative diseases, there is often a prolonged period without noticeable impairments during their initiation. Since severe cognitive deficit or vision loss takes place after that period there is an opportunity to harness endogenous protective mechanisms as potential therapeutic approaches. The activation of the biosynthesis of the docosanoid mediator neuroprotectin D1 (NPD1) is an early response to the upsurge of protein misfolding and other neuroinflammatory events. This overview discusses the potent neuroprotective and inflammation-modulating bioactivity of NPD1. This lipid mediator represents an early response to neurodegenerations, aiming to restore homeostasis.
神经退行性疾病包含复杂的细胞信号紊乱,这些紊乱最初会损害神经元回路和突触。由于为了对抗神经退行性疾病的发生而采取了多种保护机制,因此在疾病开始时通常会有一段很长的时间没有明显的损伤。由于在这段时间之后会出现严重的认知缺陷或视力丧失,因此有机会利用内源性保护机制作为潜在的治疗方法。二十二碳六烯酸介质神经保护素 D1(NPD1)的生物合成的激活是对蛋白质错误折叠和其他神经炎症事件激增的早期反应。这篇综述讨论了 NPD1 的强大的神经保护和炎症调节生物活性。这种脂质介质代表了对神经退行性变的早期反应,旨在恢复体内平衡。