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【公司名稱】 廣州健侖生物科技有限公司
【市場部】    楊永漢

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【騰訊  】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-103室

“垃圾從神經元轉移到神經膠質細胞的標準流程的發(fā)現(xiàn)，zui有可能是理解大腦和神經退行性或代謝紊亂的與年齡相關的衰退功能的關鍵，” Marsh-Armstrong說。“我們希望在生物醫(yī)學的其他領域上也有一樣重要的影響。”
研究人員仔細地觀察小鼠的視網膜神經節(jié)細胞的軸突，這一種類型的神經元從眼睛傳送視覺信息到大腦。結合*顯微鏡和Ellisman和Marsh-Armstrong實驗室開發(fā)的分子生物技術，他們發(fā)現(xiàn)，視網膜神經節(jié)細胞的受損線粒體脫落在ONH中。這些線粒體由相鄰的星形膠質細胞吸收和降解。
這項研究抗原抗體了傳統(tǒng)的觀點，即細胞內部分離，降解和去除損壞的細胞器，這個過程通常被稱為自噬(希臘語為“自吃”)。當這個過程涉及線粒體時，它被稱為線粒體自噬。Marsh-Armstrong， Ellisman和其同事們所描述的這個過程被命名為“transmitophagy”。
Ellisman說，這一發(fā)現(xiàn)可能提高對各種疾病的認識，zui終也許為各種疾病的治療提供線索。“線粒體在軸突的健康中有著顯著的作用。優(yōu)*一步探索transmitophagy發(fā)生了什么，以及這一現(xiàn)象的缺陷是否導致神經元功能障礙或疾病。”

"The discovery of the standard flow of trash from neurons to glial cells is most likely the key to understanding the age-related decline of brain and neurodegenerative or metabolic disorders," said Marsh-Armstrong. "We hope there will be equally important implications in other areas of biomedicine."
Researchers carefully examined the axons of retinal ganglion cells in mice, a type of neuron that sends visual information from the eye to the brain. Combined with advanced microscopy and molecular biology developed by Ellisman and Marsh-Armstrong Laboratories, they found that impaired mitochondrial detachment of retinal ganglion cells in ONH. These mitochondria are absorbed and degraded by adjacent astrocytes.
This study of antigen-antibody has the traditional view that the internal separation of cells, degradation and removal of damaged organelles, this process is often referred to as autophagy (Greek for "self-eating"). When this process involves mitochondria, it is called mitochondrial autophagy. The process described by Marsh-Armstrong, Ellisman and colleagues was named "transmitophagy."
Ellisman said the finding may raise awareness of various diseases and may eventually provide clues to the treatment of various diseases. "Mitochondria play a significant role in the health of axons, giving priority to further exploration of what happens to transmitophagy, and whether the flaws in this phenomenon lead to neuronal dysfunction or disease."