Government Medical College and Hospital, Sector 32, Chandigarh, India.
Mol Neurobiol. 2013 Aug;48(1):186-9. doi: 10.1007/s12035-013-8416-8. Epub 2013 Feb 10.
The eyes are the window of the brain; various pathologies of the eyes can be explained on the basis of neurological disorders and vice versa. Today, our only approach for the management of glaucoma is intraocular pressure (IOP) reduction, whether by pharmacological or surgical methods. Available methods may effectively control IOP but fall short of stopping the progression of glaucoma. IOP is just one of the risk factors our therapy addresses, so we need to work towards shifting our approach towards addressing other factors involved in the etiopathogenesis of the disease. Pathogenesis of glaucoma at molecular level can be compared with that of common neurodegenerative diseases like Alzheimer's and Parkinsonism. Targets for therapeutic intervention in chronic neurodegenerative diseases and glaucoma include apoptosis, axonal transport, free radical damage, role of polyunsaturated fatty acids, chaperones, gene regulation, etc. p38MAPK is a common pathway involved in all the neurodegenerative disease and glaucoma as well, and more research in this direction can be really beneficial for the development of novel diagnostic and therapeutic measures.
眼睛是大脑的窗户;各种眼部疾病可以根据神经紊乱来解释,反之亦然。目前,我们对青光眼的治疗方法仅为降低眼内压(IOP),无论是通过药物还是手术方法。现有的方法可能有效控制 IOP,但无法阻止青光眼的进展。IOP 只是我们治疗中针对的一个风险因素,因此我们需要努力改变方法,针对疾病发病机制中的其他因素。青光眼在分子水平上的发病机制可以与常见的神经退行性疾病(如阿尔茨海默病和帕金森病)相媲美。慢性神经退行性疾病和青光眼的治疗靶点包括细胞凋亡、轴突运输、自由基损伤、多不饱和脂肪酸的作用、伴侣蛋白、基因调控等。p38MAPK 是所有神经退行性疾病和青光眼共有的通路,在这方面进行更多的研究对于开发新的诊断和治疗措施非常有益。