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1、NRR-D-15-00053 Adriana Di Polo新闻树突的病理学变化与神经退行性变树突在成体神经元中能长时间保持稳定状态，如果稳定性发生变化，将导致树突结构和连接失常。研究已表明，在一些精神疾病和神经变性条件下，树突已发生异常或者突触损失。然而，成人脑损伤如何加速了树突缺陷的机制还未明确。加拿大蒙特利尔大学Adriana Di Polo 教授研究小组研究了在致盲疾病，如青光眼死亡的视网膜神经节细胞树突病变的机制。研究人员发现，视网膜神经节细胞损伤后，导致了树突快速回缩和分支丢失。视神经损伤增加视网膜神经节细胞内发育和DNA损伤调控蛋白2 (REDD2)的表达，抑制了哺乳动物雷帕霉素
2、靶蛋白活性。当把抗REDD2小干扰RNA（siRNA）注入受损眼内，增加的哺乳动物雷帕霉素靶蛋白使视网膜神经节细胞树突细胞恢复功能，恢复光感反应，并延长细胞的存活。这些调查结果确定，哺乳动物雷帕霉素靶蛋白通路是维持受损神经元树突稳定的重要调节器。Article: Dendrite pathology and neurodegeneration: focus on mTOR by Adriana Di Polo (Department of Neuroscience and Centre de recherche du Centre hospitalier de lUniversit de Mo
3、ntral (CRCHUM), University of Montreal, Montreal, Quebec H3R 2T6, Canada)Di Polo A (2015) Dendrite pathology and neurodegeneration: focus on mTOR. Neural Regen Res 10(4):559-561.欲获更多资讯：Neural Regen ResTitle: Dendrite pathology and neurodegeneration: focus on mTOR Summary statement: Dendrites are ext
4、remely fine branches on neurons that receive and integrate incoming neural information. Early pathological changes in dendrites are thought to contribute to neuronal dysfunction and cell death in neurodegenerative conditions such as Alzheimers disease and glaucoma. Researchers at the University of M
5、ontreal found that increasing the activity of a protein called mTOR, known to regulate cell growth and protein synthesis, restores the stability and function of dendrites in damaged neurons. Body: In adult neurons, dendrites are extremely stable and do not change over long periods of time. Loss of s
6、tability leads to defects in dendritic structure and connectivity. Indeed, dendritic abnormalities and loss of synapses have been reported in a number of psychiatric and neurodegenerative conditions. However, little is known about the mechanisms that promote dendritic defects in the adult injured br
7、ain. A research team at the University of Montreal (Quebec, Canada) led by Prof. Adriana Di Polo investigated the mechanisms underlying dendritic pathology in retinal ganglion cells, the neurons that die in prevalent blinding diseases such as glaucoma. The authors found that injury to the optic nerv
8、e, which damages retinal ganglion cell axons, led to rapid dendrite retraction and branch loss. Optic nerve lesion triggered upregulation of a stress response protein called REDD2 (regulated in development and DNA damage 2), which then inhibited the activity of mTOR (mammalian target of rapamycin),
9、a critical regulator of dendrite development. When a small interfering RNA (siRNA) against REDD2 was injected into the eye, the ensuing increase in mTOR function fully rescued retinal ganglion cell dendritic arbors, restored light-triggered responses, and extended cell survival. These findings ident
10、ify the mTOR pathway as an important regulator of dendritic arbor stability in injured neurons. The perspective article is published in Neural Regeneration Research (Vol. 10, No. 4, 2015).Article: Dendrite pathology and neurodegeneration: focus on mTOR by Adriana Di Polo (Department of Neuroscience and Centre de recherche du Centre hospitalier de lUniversit de Montral (CRCHUM), University of Montreal, Montreal, Quebec H3R 2T6, Canada)Di Polo A (2015) Dendrite pathology and neurodegeneration: focus on mTOR. Neural Regen Res 10(4):559-561.