BETA-AMYLOID PRECURSOR PROTEIN AND BRAIN DAMAGE

描述：(申请人摘要)有一种担忧，即 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的发展 在一些脑外伤和脑缺血的幸存者身上。因此，它是重要的 要了解在什么条件下增加了这一表达 蛋白质可以被调节，因此它不会对大脑产生毒性 细胞。通过在细胞水平上了解这种机制，研究- 可以开发基于治疗的方法来中断导致 对缺血损伤后神经元功能障碍和死亡的影响 无论是行为上的还是解剖学上的恢复，都可以最大化。它是 假设从大脑中恢复可以通过操作 调控β-淀粉样蛋白相互作用的外部环境 前体蛋白的表达和对伤害的分子反应。在……里面 β-淀粉样蛋白研究的第一阶段、时间进程和峰值表达 对伤害的前体和分子反应将被研究与 环境操纵。在第二阶段，调制的影响 脑缺血后β-淀粉样前体蛋白对神经元的影响 我们将考察可塑性和认知能力的改善。

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.