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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 迄今为止，AD 的治疗方案主要集中在改变神经递质系统，以最大限度地提高受疾病破坏的神经元回路的剩余活性。 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最终减缓疾病进展。 AD 神经变性的确切原因是目前神经科学中研究最深入的问题之一，最近的进展，特别是在家族性 AD 的遗传连锁方面，强烈表明 β-淀粉样蛋白 (A?) 可能是致病因素。 多个论点支持干预 A？代谢和/或清除作为 AD 治疗方法： (1) 所有已知的 AD 遗传相关形式都直接影响 Aβ 的产生或沉积； （2）在AD中，A？清除似乎受到损害； (3)AD被定义为由Aβ沉积引起的淀粉样变性。在其他淀粉样蛋白形成疾病中，已表明限制淀粉样蛋白的产生可导致其清除并引起临床改善。