{"title":"干细胞通过神经营养素的作用减缓阿尔茨海默病的认知能力下降","authors":"R. Mulvey","doi":"10.1093/BIOHORIZONS/HZU013","DOIUrl":null,"url":null,"abstract":"Alzheimer’s disease is a growing concern with no satisfactory current treatment solution. Contemporary stem cell research offers a new arena for development in this field. Transplantation of stem cells into the damaged brain brings hope of repair to damaged neurons. This appears to operate via a ‘bystander effect’ whereby neurotrophins secreted by the cells act as a neuro protectant, rather than a cell replacement mechanism as some have postulated. Such treatments can slow or even reverse cognitive decline. Research into neural stem cell transplantation has shown reversal of cognitive decline in animal models of disease via the mechanism of brain-derived neurotrophic factor secretion. Studies using nerve growth factor secreting stem cells have showed promising results with cognitive decline reversed in animal models of the disease. A Phase 1 clinical trial also showed promising reversal of cognitive decline in human subjects using transplantation of nerve growth factor secreting fibroblasts. Mesenchymal stem cells have also shown promise, and results from human trials are awaited. Induced pluripotent stem cells have provided a successful model of human disease in vitro. Although early results from transplant studies are encouraging, a lot more research will be needed before these preliminary advances can be translated to therapies with a strong evidence base to be used in practice.","PeriodicalId":52095,"journal":{"name":"Bioscience Horizons","volume":"7 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/BIOHORIZONS/HZU013","citationCount":"2","resultStr":"{\"title\":\"Stem cells slow cognitive decline in Alzheimer's disease via neurotrophin action\",\"authors\":\"R. Mulvey\",\"doi\":\"10.1093/BIOHORIZONS/HZU013\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Alzheimer’s disease is a growing concern with no satisfactory current treatment solution. Contemporary stem cell research offers a new arena for development in this field. Transplantation of stem cells into the damaged brain brings hope of repair to damaged neurons. This appears to operate via a ‘bystander effect’ whereby neurotrophins secreted by the cells act as a neuro protectant, rather than a cell replacement mechanism as some have postulated. Such treatments can slow or even reverse cognitive decline. Research into neural stem cell transplantation has shown reversal of cognitive decline in animal models of disease via the mechanism of brain-derived neurotrophic factor secretion. Studies using nerve growth factor secreting stem cells have showed promising results with cognitive decline reversed in animal models of the disease. A Phase 1 clinical trial also showed promising reversal of cognitive decline in human subjects using transplantation of nerve growth factor secreting fibroblasts. Mesenchymal stem cells have also shown promise, and results from human trials are awaited. Induced pluripotent stem cells have provided a successful model of human disease in vitro. Although early results from transplant studies are encouraging, a lot more research will be needed before these preliminary advances can be translated to therapies with a strong evidence base to be used in practice.\",\"PeriodicalId\":52095,\"journal\":{\"name\":\"Bioscience Horizons\",\"volume\":\"7 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1093/BIOHORIZONS/HZU013\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bioscience Horizons\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/BIOHORIZONS/HZU013\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Agricultural and Biological Sciences\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bioscience Horizons","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/BIOHORIZONS/HZU013","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Agricultural and Biological Sciences","Score":null,"Total":0}
Stem cells slow cognitive decline in Alzheimer's disease via neurotrophin action
Alzheimer’s disease is a growing concern with no satisfactory current treatment solution. Contemporary stem cell research offers a new arena for development in this field. Transplantation of stem cells into the damaged brain brings hope of repair to damaged neurons. This appears to operate via a ‘bystander effect’ whereby neurotrophins secreted by the cells act as a neuro protectant, rather than a cell replacement mechanism as some have postulated. Such treatments can slow or even reverse cognitive decline. Research into neural stem cell transplantation has shown reversal of cognitive decline in animal models of disease via the mechanism of brain-derived neurotrophic factor secretion. Studies using nerve growth factor secreting stem cells have showed promising results with cognitive decline reversed in animal models of the disease. A Phase 1 clinical trial also showed promising reversal of cognitive decline in human subjects using transplantation of nerve growth factor secreting fibroblasts. Mesenchymal stem cells have also shown promise, and results from human trials are awaited. Induced pluripotent stem cells have provided a successful model of human disease in vitro. Although early results from transplant studies are encouraging, a lot more research will be needed before these preliminary advances can be translated to therapies with a strong evidence base to be used in practice.