BETA-AMYLOID PRECURSOR PROTEIN AND BRAIN DAMAGE

β-淀粉样前体蛋白与脑损伤

• 批准号: 2777665
• 负责人: TERESITA L BRIONES
• 金额: $ 2.62万
• 依托单位: UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-03-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2777665
• 关键词: amyloid proteins; cerebral ischemia /hypoxia; laboratory rat; molecular pathology; neural plasticity

DESCRIPTION: (Applicant's abstract) There is a concern that prolonged beta-amyloid precursor protein expression following injury might actively contribute to the development of Alzheimer-like pathology seen in some survivors of TBI and cerebral ischemia. Thus it is important to understand the conditions under which increased expression of this protein can be modulated so that it does not become toxic to the brain cells. By understanding this mechanism at the cellular level, research- based treatment can be developed to interrupt the processes that lead to the dysfunction and death of neurons after ischemic injury so that recovery, behavioral and anatomical, can be maximized. It is hypothesized that recovery from cerebral can be achieved by manipulating the external environment to modulate the interplay between beta-amyloid precursor protein expression and the molecular responses to injury. In phase one of the study, time course and peak expression of beta-amyloid precursor and molecular responses to injury will be examined in relation to environmental manipulation. In phase two, the effects of modulated levels of beta-amyloid precursor protein aften ischemia on neuronal plasticity and cognitive improvement will be examined.

描述：（申请人的摘要） 损伤后β-淀粉样前体蛋白的表达可能 积极促进阿尔茨海默病样病理学的发展， 在一些脑外伤和脑缺血的幸存者中。 因此， 为了了解这种表达增加的条件， 可以调节蛋白质，使其不会对大脑有毒 细胞 通过在细胞水平上理解这种机制，研究- 可以开发基于治疗的方法来中断导致 缺血性损伤后神经元的功能障碍和死亡， 可以最大限度地恢复行为和解剖。 是 假设大脑的恢复可以通过操纵 外部环境调节β-淀粉样蛋白 前体蛋白表达和对损伤的分子反应。 在 研究的第一阶段，β-淀粉样蛋白的时间进程和峰值表达 将检查损伤的前体和分子反应与 到环境操控 在第二阶段，调制的影响 脑缺血后神经元β-淀粉样前体蛋白水平 将检查可塑性和认知改善。