A. Keskin, Nazlı Durmaz, G. Uncu, E. Erzurumluoglu, Z. Yıldırım, N. Tuncer, D. O. Adapınar
{"title":"阿尔茨海默病的未来治疗","authors":"A. Keskin, Nazlı Durmaz, G. Uncu, E. Erzurumluoglu, Z. Yıldırım, N. Tuncer, D. O. Adapınar","doi":"10.5772/INTECHOPEN.85096","DOIUrl":null,"url":null,"abstract":"Alzheimer’s disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer’s disease (AD) are extracellular Amyloid beta (A β ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with A β plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modi-fying therapies for AD that are currently being studied in phase I–III trials.","PeriodicalId":91314,"journal":{"name":"Journal of geriatric medicine and gerontology","volume":"4999 3 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":"{\"title\":\"Future Treatment of Alzheimer Disease\",\"authors\":\"A. Keskin, Nazlı Durmaz, G. Uncu, E. Erzurumluoglu, Z. Yıldırım, N. Tuncer, D. O. Adapınar\",\"doi\":\"10.5772/INTECHOPEN.85096\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Alzheimer’s disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer’s disease (AD) are extracellular Amyloid beta (A β ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with A β plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modi-fying therapies for AD that are currently being studied in phase I–III trials.\",\"PeriodicalId\":91314,\"journal\":{\"name\":\"Journal of geriatric medicine and gerontology\",\"volume\":\"4999 3 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-05-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of geriatric medicine and gerontology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5772/INTECHOPEN.85096\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of geriatric medicine and gerontology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.85096","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Alzheimer’s disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer’s disease (AD) are extracellular Amyloid beta (A β ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with A β plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modi-fying therapies for AD that are currently being studied in phase I–III trials.