CLINICAL TRIAL: PHASE 3 MULTICENTER, RANDOMIZED, DOUBLE BLIND, PLACEBO CONTROLLE

临床试验：第 3 阶段多中心、随机、双盲、安慰剂对照

• 批准号: 7725006
• 负责人: RUTH MULNARD MCCARGAR
• 金额: $ 0.05万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-12-01 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7725006
• 关键词: Address; Affect; Amyloid Proteins; Amyloid beta-Protein; Amyloidosis; Clinical; Computer Retrieval of Information on Scientific Projects Database; Deposition; Disease; Disease Progression; Double-Blind Method; Funding; Grant; Institution; Intervention; Link; Metabolism; Modification; Nerve Degeneration; Neurons; Neurosciences; Neurotransmitters; Patients; Phase III Clinical Trials; Placebos; Presenile Alzheimer Dementia; Process; Production; Randomized; Research; Research Personnel; Resources; Source; System; Therapeutic; United States National Institutes of Health; base; genetic linkage

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The therapeutic options for treatment of AD have thus far focused on modifications of neurotransmitter systems to maximize the remaining activity in neuronal circuits ravaged by the disease. Neurotransmitter-based approaches may provide transient symptomatic benefit for some patients, but do not address the underlying disease process or, ultimately, slow disease progression. The precise cause of the neurodegeneration in AD is currently one of the most intensely investigated issues in neuroscience, and recent advances, in particular, in genetic linkage of familial AD, have strongly suggested that the beta-amyloid protein (A?) may be the causative agent. Multiple arguments support intervention in A? metabolism and/or clearance as a therapeutic approach to the treatment of AD: (1) All known genetically linked forms of AD directly affect either production or deposition of A?; (2) in AD, A? clearance appears to be impaired; and (3) AD is defined as an amyloidosis by the deposition of A?. In other amyloidogenic diseases, it has been shown that limiting production of the amyloid protein leads to its clearance and induces clinical improvement.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 迄今为止，用于治疗AD的治疗方法的重点是神经递质系统的修饰，以最大程度地提高疾病破坏的神经元电路的剩余活性。 基于神经递质的方法可能会为某些患者提供短暂的症状益处，但不能解决潜在的疾病过程，或者最终疾病进展缓慢。当前，AD神经退行性的确切原因是神经科学中最深入研究的问题之一，最近的进步，尤其是家族性AD的遗传联系，强烈建议β-淀粉样蛋白（A？）可能是β-淀粉样蛋白（A？）。 多个论点支持干预？代谢和/或清除是一种治疗AD治疗的治疗方法：（1）所有已知的遗传联系形式的AD形式直接影响A？的生产或沉积； （2）在广告中，一个？清除似乎受到损害； （3）AD通过A？的沉积将AD定义为淀粉样变性。在其他淀粉样蛋白疾病中，已经表明，限制淀粉样蛋白的产生会导致其清除并诱导临床改善。