Brent R Kisby, Juliet T. Jarrell, M. Agar, David S. Cohen, Eric R Rosin, C. Cahill, J. Rogers, Xudong Huang
{"title":"阿尔茨海默病及其潜在的替代疗法","authors":"Brent R Kisby, Juliet T. Jarrell, M. Agar, David S. Cohen, Eric R Rosin, C. Cahill, J. Rogers, Xudong Huang","doi":"10.4172/2161-0460.1000477","DOIUrl":null,"url":null,"abstract":"Alzheimer’s Disease (AD) is a chronic neurodegenerative disease that affects over 5 million individuals in the United States alone. Currently, there are only two kinds of pharmacological interventions available for symptomatic relief of AD; Acetyl Cholinesterase Inhibitors (AChEI) and N-methyl-D-aspartic Acid (NMDA) receptor antagonists and these drugs do not slow down or stop the progression of the disease. Several molecular targets have been implicated in the pathophysiology of AD, such as the tau (τ) protein, Amyloid-beta (Aβ), the Amyloid Precursor Protein (APP) and more and several responses have also been observed in the advancement of the disease, such as reduced neurogenesis, neuroinflammation, oxidative stress and iron overload. In this review, we discuss general features of AD and several small molecules across different experimental AD drug classes that have been studied for their effects in the context of the molecular targets and responses associated with the AD progression. These drugs include: Paroxetine, Desferrioxamine (DFO), N-acetylcysteine (NAC), Posiphen/-(−)Phenserine, JTR-009, Carvedilol, LY450139, Intravenous immunoglobulin G 10%, Indomethacin and Lithium Carbonate (Li2CO3).","PeriodicalId":15013,"journal":{"name":"Journal of Alzheimer's disease & Parkinsonism","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"15","resultStr":"{\"title\":\"Alzheimer’s Disease and Its Potential Alternative Therapeutics\",\"authors\":\"Brent R Kisby, Juliet T. Jarrell, M. Agar, David S. Cohen, Eric R Rosin, C. Cahill, J. Rogers, Xudong Huang\",\"doi\":\"10.4172/2161-0460.1000477\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Alzheimer’s Disease (AD) is a chronic neurodegenerative disease that affects over 5 million individuals in the United States alone. Currently, there are only two kinds of pharmacological interventions available for symptomatic relief of AD; Acetyl Cholinesterase Inhibitors (AChEI) and N-methyl-D-aspartic Acid (NMDA) receptor antagonists and these drugs do not slow down or stop the progression of the disease. Several molecular targets have been implicated in the pathophysiology of AD, such as the tau (τ) protein, Amyloid-beta (Aβ), the Amyloid Precursor Protein (APP) and more and several responses have also been observed in the advancement of the disease, such as reduced neurogenesis, neuroinflammation, oxidative stress and iron overload. In this review, we discuss general features of AD and several small molecules across different experimental AD drug classes that have been studied for their effects in the context of the molecular targets and responses associated with the AD progression. These drugs include: Paroxetine, Desferrioxamine (DFO), N-acetylcysteine (NAC), Posiphen/-(−)Phenserine, JTR-009, Carvedilol, LY450139, Intravenous immunoglobulin G 10%, Indomethacin and Lithium Carbonate (Li2CO3).\",\"PeriodicalId\":15013,\"journal\":{\"name\":\"Journal of Alzheimer's disease & Parkinsonism\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"15\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Alzheimer's disease & Parkinsonism\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4172/2161-0460.1000477\",\"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 Alzheimer's disease & Parkinsonism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2161-0460.1000477","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 15
摘要
阿尔茨海默病(AD)是一种慢性神经退行性疾病,仅在美国就有超过500万人受到影响。目前,只有两种药物干预可以缓解AD的症状;乙酰胆碱酯酶抑制剂(AChEI)和n -甲基- d -天冬氨酸(NMDA)受体拮抗剂以及这些药物不能减缓或阻止疾病的进展。一些分子靶点与AD的病理生理有关,如tau (τ)蛋白,淀粉样蛋白- β (Aβ),淀粉样蛋白前体蛋白(APP),以及在疾病进展中观察到的更多反应,如神经发生减少,神经炎症,氧化应激和铁过载。在这篇综述中,我们讨论了阿尔茨海默病的一般特征,以及不同实验阿尔茨海默病药物类别中的几种小分子,这些小分子在与阿尔茨海默病进展相关的分子靶点和反应中的作用已经被研究。这些药物包括:帕罗西汀、地铁胺(DFO)、n -乙酰半胱氨酸(NAC)、波西芬/-(−)苯丝氨酸、JTR-009、卡维地洛、LY450139、静脉注射免疫球蛋白g10%、吲哚美辛和碳酸锂(Li2CO3)。
Alzheimer’s Disease and Its Potential Alternative Therapeutics
Alzheimer’s Disease (AD) is a chronic neurodegenerative disease that affects over 5 million individuals in the United States alone. Currently, there are only two kinds of pharmacological interventions available for symptomatic relief of AD; Acetyl Cholinesterase Inhibitors (AChEI) and N-methyl-D-aspartic Acid (NMDA) receptor antagonists and these drugs do not slow down or stop the progression of the disease. Several molecular targets have been implicated in the pathophysiology of AD, such as the tau (τ) protein, Amyloid-beta (Aβ), the Amyloid Precursor Protein (APP) and more and several responses have also been observed in the advancement of the disease, such as reduced neurogenesis, neuroinflammation, oxidative stress and iron overload. In this review, we discuss general features of AD and several small molecules across different experimental AD drug classes that have been studied for their effects in the context of the molecular targets and responses associated with the AD progression. These drugs include: Paroxetine, Desferrioxamine (DFO), N-acetylcysteine (NAC), Posiphen/-(−)Phenserine, JTR-009, Carvedilol, LY450139, Intravenous immunoglobulin G 10%, Indomethacin and Lithium Carbonate (Li2CO3).