Department of Pathology, Waisman Center for Developmental Disabilities, UWMadison, WI, USA.
Curr Alzheimer Res. 2010 May;7(3):200-6. doi: 10.2174/156720510791050957.
As the mechanisms underlying neuronal development and degeneration become clarified, a number of common effectors and signaling pathways are becoming apparent. Here we describe the identification of Abeta, long considered a pathologic mediator of Alzheimers Disease and Down Syndrome, as similarly over-expressed in the neurodevelopmental disease, Fragile X Syndrome. We also show that mGluR5 inhibitors, currently employed for the treatment of Fragile X, reduce Abeta production in rodent models of Fragile X and AD as well as reduce disease phenotypes including seizures. Thus seemingly disparate neurologic diseases may share a common pathologic instigator and be treatable with a common, currently available class of therapeutics.
随着神经元发育和退化机制的阐明，一些共同的效应器和信号通路逐渐显现出来。在这里，我们描述了 Abeta 的鉴定，Abeta 长期以来被认为是阿尔茨海默病和唐氏综合征的病理介质，在神经发育疾病脆性 X 综合征中也有类似的过度表达。我们还表明，mGluR5 抑制剂目前用于治疗脆性 X 综合征，可减少脆性 X 综合征和 AD 啮齿动物模型中的 Abeta 产生，并减少包括癫痫发作在内的疾病表型。因此，看似不同的神经疾病可能具有共同的病理触发因素，并可采用一种共同的、目前可用的治疗药物进行治疗。
