Department of Pharmaceutical Sciences, Northeastern Ohio Universities Colleges of Medicine and Pharmacy, Rootstown, OH 44272, USA.
Neuroscience. 2011 Mar 10;176:1-11. doi: 10.1016/j.neuroscience.2010.12.036. Epub 2010 Dec 25.
Glaucoma is an age-related optic neuropathy involving sensitivity to ocular pressure. The disease is now seen increasingly as one of the central nervous system, as powerful new approaches highlight an increasing number of similarities with other age-related neurodegenerations such as Alzheimer's and Parkinson's. While the etiologies of these diseases are diverse, they involve many important common elements including compartmentalized programs of degeneration targeting axons, dendrites and finally cell bodies. Most age-related degenerations display early functional deficits that precede actual loss of neuronal substrate. These are linked to several specific neurochemical cascades that can be linked back to dysregulation of Ca(2+)-dependent processes. We are now in the midst of identifying similar cascades in glaucoma. Here we review recent evidence on the pathological progression of neurodegeneration in glaucoma and some of the Ca(2+)-dependent mechanisms that could underlie these changes. These mechanisms present clear implications for efforts to develop interventions targeting neuronal loss directly and make glaucoma an attractive model for both interrogating and informing other neurodegenerative diseases.
青光眼是一种与年龄相关的视神经病变，涉及对眼内压的敏感性。如今，这种疾病越来越被视为中枢神经系统疾病之一，因为强有力的新方法强调了与其他与年龄相关的神经退行性疾病（如阿尔茨海默病和帕金森病）越来越多的相似之处。尽管这些疾病的病因各不相同，但它们涉及许多重要的共同要素，包括针对轴突、树突和最终细胞体的退化分区程序。大多数与年龄相关的退行性变表现出早期的功能缺陷，这些缺陷先于神经元基质的实际丧失。这些与几种特定的神经化学级联反应有关，这些级联反应可以追溯到 Ca(2+)-依赖性过程的失调。我们现在正处于确定青光眼的类似级联反应的过程中。在这里，我们回顾了青光眼神经退行性病变的病理进展的最新证据，以及可能是这些变化基础的一些 Ca(2+)-依赖性机制。这些机制对旨在直接针对神经元丧失的干预措施的发展具有明显的意义，并使青光眼成为研究和为其他神经退行性疾病提供信息的理想模型。
