CLINICAL TRIAL: EVALUATION OF THE SAFETY, TOLERABILITY AND IMPACT ON BIOMARKERS

临床试验：评估安全性、耐受性和对生物标志物的影响

• 批准号: 7725024
• 负责人: RUTH MULNARD MCCARGAR
• 金额: $ 0.32万
• 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/7725024
• 关键词: Acetylcholinesterase Inhibitors; Activities of Daily Living; Alzheimer' s Disease; Amyloid; Amyloid beta-Protein; Brain; Cognitive; Computer Retrieval of Information on Scientific Projects Database; Degenerative Disorder; Dementia; Deposition; Disease; Elderly; Etiology; Facilities and Administrative Costs; Funding; Grant; Institution; Lead; Life Expectancy; Link; Memantine; Memory Loss; Nerve Degeneration; Neurons; Neurotransmitters; Public Health; Research; Research Personnel; Resources; Source; System; Thinking; Toxic effect; United States National Institutes of Health; prevent

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. Alzheimer's Disease (AD), a progressive degenerative disease of the brain resulting in impaired memory and loss of cognitive and functional abilities, is the most common cause of dementia in the elderly. It poses a huge public health problem, particularly as life expectancy continues to increase. In the US, the direct and indirect costs of AD were estimated at over $100 billion per year (Ernst 1994). Currently approved treatment for AD includes acetylcholinesterase inhibitors and memantine, both of which target neurotransmitter systems and show symptomatic benefits. There is no disease-modifying treatment to prevent AD or to slow its progression. A major hypothesis about the etiology of AD is that beta-amyloid (A?) aggregates and is deposited in the brain, which leads to neuronal damage and ultimately to AD (reviewed in Hardy 1997). A? ending at residue 42 (A?42) is thought to be the key initiator because A?42 predominates in early amyloid deposits in the brain and has a greater propensity to aggregate, form fibrils, and lead to cellular toxicity than A? ending at residue 40 (A?40) or shorter forms of A?. Oxidative damage is a key factor implicated in the neurodegeneration of AD (Behl 1999) and can be linked to A? (Pratico 1999, Lustbader 2004).

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